#NF-κB pathway

[blueoaknx]

Mitochondrial Dysfunction in Endometriosis

 A Technical Overview of Cellular Mechanisms

Endometriosis, a common gynecological condition affecting approximately 10% of women during their reproductive years, is characterized by the presence of endometrial-like tissue outside the uterine cavity, most frequently in the ovaries, fallopian tubes, and peritoneal cavity. This ectopic tissue leads to a chronic inflammatory environment, pain, and infertility. While the pathophysiology of endometriosis is not fully understood, recent studies have increasingly highlighted mitochondrial dysfunction as a central feature of the disease. This technical article provides a detailed exploration of the role of mitochondria in endometriosis, examining the molecular and cellular mechanisms through which mitochondrial dysfunction contributes to disease progression.

Mitochondrial Function and Metabolism

Mitochondria are dynamic organelles responsible for numerous vital cellular processes, most notably ATP production through oxidative phosphorylation (OXPHOS). ATP is generated within the mitochondrial matrix by the electron transport chain (ETC), which involves the transfer of electrons from NADH and FADH2 to oxygen molecules, ultimately producing ATP. In addition to ATP production, mitochondria are involved in the regulation of calcium signaling, the maintenance of cellular redox balance, apoptosis, and the synthesis of key metabolites, including lipids and steroids. Mitochondria also contain their own genome (mitochondrial DNA or mtDNA), which encodes essential components of the ETC and mitochondrial protein synthesis machinery.

Mitochondria maintain their function through a balance of fusion and fission, processes that help ensure the organelle's shape, distribution, and response to stress. Mitochondrial dysfunction can arise from an imbalance in these processes, as well as from damage to mitochondrial DNA (mtDNA), excessive reactive oxygen species (ROS) production, and impaired bioenergetic functions. In the context of endometriosis, these disruptions have profound implications for cellular homeostasis and tissue function.

Mitochondrial Dysfunction in Endometriosis

In endometriosis, altered mitochondrial function contributes significantly to the disease's pathology. The following mechanisms are central to understanding how mitochondrial dysfunction drives the progression of endometriosis:

1. Altered Metabolic Shifts: The Warburg Effect

A hallmark of cancerous and proliferative cells is a shift in cellular metabolism, often referred to as the Warburg effect, in which cells preferentially utilize glycolysis over oxidative phosphorylation for ATP production, even in the presence of oxygen. This metabolic reprogramming is also observed in endometriotic cells, particularly in ectopic lesions, where cells exhibit increased glycolytic activity. In these lesions, endometrial cells rely less on mitochondrial OXPHOS and instead preferentially use glycolysis for ATP production, generating lactate as a byproduct.

This metabolic shift supports enhanced cell proliferation and survival under suboptimal conditions, characteristic of the hyperplastic nature of endometriosis. Glycolysis is less efficient in terms of ATP production compared to OXPHOS, yet it provides the necessary metabolic intermediates for cell division and biosynthesis. Additionally, the accumulation of lactate in the extracellular space lowers the local pH, which can exacerbate tissue inflammation and create a microenvironment conducive to the growth and persistence of ectopic lesions.

2. Mitochondrial DNA Damage and Instability

Mitochondria are highly susceptible to damage due to their proximity to ROS-producing processes in the electron transport chain. ROS, which are byproducts of cellular respiration, can damage mitochondrial lipids, proteins, and most notably, mitochondrial DNA (mtDNA). Unlike nuclear DNA, mtDNA is not protected by histones, making it particularly vulnerable to oxidative damage. In endometriosis, there is compelling evidence that mtDNA is significantly damaged in ectopic endometrial tissue. Studies have shown mtDNA deletions, mutations, and increased levels of mtDNA fragmentation in these tissues, which suggest a breakdown in the integrity of mitochondrial function.

The damaged mtDNA further exacerbates mitochondrial dysfunction, impairing the ability of mitochondria to generate ATP through OXPHOS. This, in turn, results in an increased reliance on anaerobic glycolysis, fueling the Warburg effect. Furthermore, mtDNA mutations can impair mitochondrial protein synthesis, leading to dysfunctional mitochondrial complexes and altered cellular bioenergetics, perpetuating a cycle of cellular dysfunction in endometriotic lesions.

3. Oxidative Stress and Inflammation

One of the critical roles of mitochondria is the regulation of cellular redox balance. Under normal conditions, mitochondria produce ROS as part of the electron transport chain. However, when mitochondrial function is compromised—whether due to damage, oxidative stress, or metabolic reprogramming—excess ROS are produced, leading to a state of oxidative stress. In endometriosis, ectopic endometrial tissue exhibits elevated levels of ROS, contributing to a persistent inflammatory environment.

Oxidative stress in endometriotic lesions is amplified by mitochondrial dysfunction and is further exacerbated by the Warburg effect, which generates additional ROS during glycolysis. ROS directly activate inflammatory pathways, particularly through the nuclear factor-kappa B (NF-κB) signaling pathway, leading to the production of pro-inflammatory cytokines such as IL-6, IL-1β, and TNF-α. These cytokines perpetuate the inflammatory response, recruiting immune cells to the site of ectopic lesions, which leads to pain, fibrosis, and the development of adhesions.

Moreover, ROS play a critical role in sensitizing nociceptors, contributing to the chronic pain experienced by women with endometriosis. The interplay between oxidative stress and inflammation forms a vicious cycle that fuels the progression of endometriosis and promotes the growth and persistence of ectopic lesions.

4. Impaired Mitochondrial Dynamics: Fragmentation and Dysfunction

Mitochondria undergo constant fusion and fission, processes that regulate mitochondrial morphology, quality control, and function. Fusion allows for the mixing of mitochondrial contents, which can help dilute damaged components, while fission helps eliminate dysfunctional mitochondria through mitophagy. In endometriosis, there is evidence of disrupted mitochondrial dynamics, particularly an increase in mitochondrial fragmentation. Fragmented mitochondria are less efficient at ATP production and more prone to accumulating damaged proteins and lipids, which further impairs mitochondrial function.

The imbalance between mitochondrial fusion and fission in endometriosis is linked to altered expression of key proteins such as mitofusins (MFN1/2) and dynamin-related protein 1 (DRP1). DRP1-mediated mitochondrial fission is upregulated in endometriotic lesions, contributing to the generation of fragmented mitochondria. These fragmented organelles are associated with increased oxidative stress, apoptosis resistance, and enhanced cell proliferation—features that contribute to the pathogenesis of endometriosis.

5. Apoptosis Resistance and Cell Survival

Mitochondria play a pivotal role in regulating apoptosis through the release of pro-apoptotic factors, such as cytochrome c, from the mitochondrial intermembrane space. These factors initiate the caspase cascade, leading to cell death. However, in endometriosis, ectopic endometrial cells exhibit resistance to apoptosis, allowing them to survive and proliferate abnormally.

Mitochondrial dysfunction in endometriosis leads to alterations in key apoptotic proteins, including Bcl-2 family members, which regulate mitochondrial outer membrane permeabilization (MOMP). The overexpression of anti-apoptotic proteins, such as Bcl-2 and Bcl-xL, and the downregulation of pro-apoptotic proteins, such as Bax and Bak, result in the persistence of damaged cells. This resistance to apoptosis allows for the survival of endometriotic lesions in hostile environments, contributing to the chronic nature of the disease and complicating treatment strategies.

Therapeutic Implications: Targeting Mitochondrial Dysfunction

Given the central role of mitochondrial dysfunction in endometriosis, therapeutic approaches targeting mitochondrial function hold promise for improving disease management. Several potential strategies include:

Antioxidant Therapies: Reducing oxidative stress through antioxidants such as N-acetylcysteine (NAC), Coenzyme Q10 (CoQ10), and vitamin E could help restore mitochondrial function and reduce inflammation in endometriotic tissues.

Modulation of Mitochondrial Dynamics: Targeting proteins involved in mitochondrial fusion and fission, such as DRP1 and MFN2, may help restore mitochondrial morphology and improve bioenergetic function in endometriotic lesions.

Inhibition of Glycolysis: Given the shift toward glycolysis in endometriotic cells, inhibiting key glycolytic enzymes, such as hexokinase or lactate dehydrogenase, may help reduce lesion growth and metabolic reprogramming.

Mitochondrial Biogenesis Stimulation: Activators of PGC-1α, a central regulator of mitochondrial biogenesis, could promote the generation of healthy mitochondria and improve overall cellular metabolism in endometriotic tissue.

Conclusion

Mitochondrial dysfunction is a key contributor to the pathogenesis of endometriosis. Alterations in mitochondrial metabolism, oxidative stress, mitochondrial DNA damage, and impaired apoptotic regulation are central to the disease's progression. Understanding the molecular mechanisms underlying mitochondrial dysfunction in endometriosis provides novel insights into potential therapeutic strategies. Targeting mitochondrial function and bioenergetics could lead to more effective treatments for endometriosis, alleviating its symptoms and improving outcomes for affected women.

[willowreader]

Inflamed from Within: How COVID-19 Ignites Heart Damage

Here is a version non-medical language terms.

Scientists recently uncovered something unsettling in a study of 54 heart tissue samples. The virus behind COVID-19 can creep into heart cells too, stirring up a storm of inflammation. These heart cells, called *cardiomyocytes*, are meant to keep our hearts beating strong, but this virus has found a way in, using the *TNF-NF-κB* pathway—a process that, when pushed too far, spells trouble.

Once inside, the virus seems to change the very way these heart cells function, flipping genetic switches that can lead to chaos. One gene, called *CXCL2*, kicks into high gear, summoning immune cells to the heart like soldiers to a battlefield. But sometimes, too many soldiers can cause more damage than they fix.

The protein at the center of this, *NF-κB*, is like the conductor of this chaotic orchestra, fueling inflammation that, if left unchecked, can weaken the heart. It’s as if the body, in trying to defend itself, starts tearing at its own foundation.

This study adds to a growing concern—COVID-19 is leaving its mark on the heart, and some of that damage may linger long after the virus has left. Scientists are sounding the alarm, and they’re urging us to take this more seriously than ever before. Posted by David It Up on X

[darkmaga-returns]

Story at-a-glance

Butyrate, a short-chain fatty acid produced when gut bacteria ferment dietary fiber, serves as both an energy source for colon cells and an important signaling molecule for immune regulation

By inhibiting histone deacetylases (HDAC) and suppressing the NF-κB pathway, butyrate acts as a powerful anti-inflammatory agent, helping prevent chronic inflammation that contributes to various diseases

Butyrate promotes regulatory T cell development while modulating other immune cells, helping maintain immune tolerance and preventing autoimmune responses while supporting balanced immune function

Butyrate plays a significant role in managing chronic diseases like IBD, multiple sclerosis and Type 2 diabetes by reducing inflammation and supporting gut barrier function

Emerging research suggests that butyrate influences brain health by modulating the gut-brain axis; it reduces neuroinflammation and supports cognitive function, and plays a supporting role in the prevention of neurological disorders like Alzheimer's disease and depression

[helen0086]

Progress in the Study of the Protective Effect and Mechanism of C-phycocyanin on Liver Injury

Abstract: C-phycocyanin (C-phycocyanin) is a pigment-containing protein from marine algae that has shown promising results in the treatment of many inflammatory diseases and tumors. C-alpha-cyanobilin is a pigment-containing protein from marine algae that has been shown to be effective in the treatment of various inflammatory diseases and tumors. C-alpha-cyanobilin has a protective effect on various liver diseases, such as drug-induced or toxic substance-induced liver damage, non-alcoholic fatty liver disease, hepatic fibrosis, and hepatic ischemia-reperfusion injury. The protective effect of C-alginin on liver injury is mainly realized through the regulation of signaling pathways such as nuclear factor (NF)-κB, phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) and AMP-dependent protein kinase (AMPK), and the inhibition of oxidative stress, etc., and is not toxic to normal cells. Therefore, C-alginin has a broad application prospect as a potential natural hepatoprotective marine active substance. In recent years, the research progress of the protective effect of C-alginin on liver injury and its mechanism is summarized.

 C-phycocyanin (C-phycocyanin) is a complex protein of cyanobacteria and a natural food protein pigment with pharmacological effects such as antioxidant, anti-inflammatory and anti-tumor effects, as well as fast-acting and low-toxicity, it can be used as a functional food [1-2]. C-Alginin can also enhance immunity and is safe, without causing acute and subacute toxic reactions [3]. Selenium-enriched PC has been shown to have stronger pharmacological effects [4]. Therefore, C-alginate has important research value both as a drug and a functional food, and has become a hot spot in the field of pharmaceutical research [5]. In this paper, we summarize the progress of research on the application and mechanism of C-alginin in liver diseases.

1 Ameliorative effect of C-phycocyanin on liver injury caused by drugs and toxic substances

The liver is the metabolic center of drugs and exogenous toxic substances, and metabolites are prone to liver injury. C-PC can inhibit the synthesis and release of inflammatory factors such as tumor necrosis factor (TNF)-α and interferon-γ, and increase the activities of catalase and superoxide dismutase (SOD), which can inhibit hepatic inflammation and alleviate hepatic injury [3]. It has been found that C-PC can significantly prevent thioacetamide-induced liver injury, significantly reduce the levels of alanine aminotransferase (ALT) and aliquot aminotransferase (AST), shorten the prothrombin time and reduce the hepatic histopathological damage, and improve the survival rate of rats with fulminant hepatic failure [6]. C-alginin also has a good effect on thioacetamide-induced hepatic encephalopathy, which can be seen in the reduction of tryptophan and lipid peroxidation indexes in different regions of the brain, and the enhancement of catalase and glutathione peroxidase activities in rats with fulminant hepatic failure [6].

Another study found that C-alginin not only attenuates the oxidative stress induced by 2-acetylaminofluorene and reduces the generation of reactive oxygen species (ROS) radicals, but also inhibits the phosphorylation of protein kinase B (Akt) and the nuclear translocation of nuclear factor (NF)-κB induced by 2-acetylaminofluorene, thus inhibiting the expression of multidrug resistance genes [7]. Osman et al. [8] also showed that C-alginin could normalize the levels of ALT, AST, catalase, urea, creatinine, SOD and glutathione-s-transferase in the livers of rats poisoned with carbon tetrachloride (CCl4). This result was also verified in human liver cell line (L02) [9]. C-phycocyanin can effectively scavenge ROS and inhibit CCl4-induced lipid peroxidation in rat liver [10], and C-PC can improve the antioxidant defense system and restore the structure of hepatocytes and hepatic enzymes in the liver of gibberellic acid-poisoned albino rats [11]. As a PC chromophore, phycocyanin can also significantly inhibit ROS generation and improve liver injury induced by a variety of drugs and toxic substances [10]. Liu et al. [12] found that phycocyanin showed strong anti-inflammatory effects in a CCl4-induced hepatic injury model in mice, which could significantly reduce the levels of ALT, AST, the expression of TNF-α and cytochrome C, increase the levels of albumin and SOD, and proliferate cytosolic nuclei. It can significantly reduce ALT and AST levels and the expression of TNF-α and cytochrome C, increase albumin levels and the expression of SOD and proliferating cell nuclear antigen, promote hepatocyte regeneration and improve the survival rate of mice with acute liver failure.

Gammoudi et al [13] used response surface method to optimize the extraction process of C-phycocyanin, and obtained high extraction recovery. C-phycocyanin extracted by the optimized method has the ability of scavenging hydroxyl, superoxide anion and nitric oxide radicals as well as the ability of metal chelating, and it has stronger antioxidant effect; C-PC significantly increased the activity of SOD and inhibited the increase of ALT, AST, and bilirubin in cadmium-poisoned rats. C-PC significantly increased the activity of SOD and inhibited the increase of ALT, AST and bilirubin in rats with cadmium poisoning. The above studies show that C-phycocyanin can effectively protect liver injury caused by drugs and toxic substances, and has the efficacy as the basis for drug development.

2 Preventive effect of C-alginin on hepatic fibrosis

Liver fibrosis is an inevitable process in the development of various chronic liver diseases and may be reversed with early and timely treatment. The key to liver fibrosis is the activation of hepatic stellate cells. Previous studies have found that low-dose C-alginin combined with soy isoflavones can inhibit hepatic stellate cell activation by inhibiting the activity of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase［14］, but it is not clear whether C-alginin alone can inhibit the activity of NADPH oxidase. Therefore, the combination of C-algin and soy isoflavones at appropriate doses may have a preventive effect on liver fibrosis in high-risk groups. C-alginin may inhibit the progression of NADPH by suppressing oxidative damage, thereby inhibiting the development of hepatic fibrosis [15].

Epithelial mesenchymal transition (EMT) is one of the key mechanisms contributing to the development of fibrotic diseases. C-alginin inhibits transforming growth factor β1 (TGF-β1)-induced human EMT [16]. Although the effect of C-alginin on EMT in hepatic fibrosis has not been reported, it has been found that C-alginin can reduce pulmonary fibrosis by inhibiting epithelial mesenchymal transition [17]. Another study found that C-alginin could reduce the expression of α-smooth muscle actin (α-SMA) and connective tissue growth factor (CTGF) mRNA in human dermal fibroblasts and alleviate fibrous contracture [18]. The results of these studies also have significance for the inhibition of hepatic fibrosis, and provide a theoretical basis for the further study of C-PC as a potential antifibrotic drug.

3 Protective effect of C-alginin on hepatic ischemia-reperfusion injury

Liver ischemia/reperfusion injury is an important clinicopathophysiological phenomenon. It was found that the addition of two different doses (0.1 g/L and 0.2 g/L) of C-alginin to the Krebs Henseleit preservation solution significantly decreased hepatic ALT, AST and alkaline phosphatase activities, and reduced the rate of lipid peroxidation and malondialdehyde content in an isolated perfused rat liver model, and increased the activities of hepatic glutathione-s-transferase and glutathione peroxidase, as well as sulfhydryl groups in hepatic tissue. On the other hand, it can increase the activities of hepatic glutathione-s-transferase and glutathione peroxidase and the content of sulfhydryl groups in liver tissues, therefore, C-alginin can significantly reduce hepatic ischemia/reperfusion injury as an antioxidant [19]. In isolated perfused mouse livers, it was found that C-alginin significantly reduced the phagocytosis and respiratory burst activity of hepatic macrophages (Kupffer cells), attenuated cytotoxicity and inflammation induced by highly active Kupffer cells, and dose-dependently inhibited carbon phagocytosis and carbon-induced oxygen uptake by perfused livers, and then inhibited the increase of hepatic nitric oxide synthase activity induced by gonadotropins [20]. and thus inhibit the thyroid hormone-induced elevation of hepatic nitric oxide synthase activity [20].

However, C-alginin has a very short half-life in vivo, which limits its application in vivo. It was found that the use of polyethylene glycol-b-(polyglutamic acid-g-polyethyleneimine), a macromolecular material with good drug-carrying capacity and slow-release properties, as a nanocarrier of C-alginin could solve this problem, and the release of C-alginin could be delayed by subcutaneous injection into the abdominal region of rats, which could attenuate islet damage caused by hepatic ischemia/reperfusion and enhance the function of the islets [21]. This study broadens the scope of application of C-alginin in vivo and improves the therapeutic effect of C-alginin.

4 Inhibitory effect of C-alginin on hepatocellular carcinoma

It was found that C-alginin significantly reduced the expression of matrix metalloproteinase (MMP)-2 and MMP-9 and the expression of tissue inhibitor of metalloproteinase 2 (TIMP2) mRNA in human hepatocellular carcinoma cells (HepG2 cells) [22]. C-alginin is a natural photosensitizer, and photodynamic therapy (PDT) mediated by alginin microcystin induced a large accumulation of ROS in HepG2 cells, which promoted mitochondrial damage and cytochrome C release, and led to apoptosis of hepatocellular carcinoma cells [23].

Liu et al. [24] used nanoscale C-alginate particles prepared by lactobionic acid grafting and adriamycin loading to enhance the growth inhibition of HepG2 cells when combined with chemo-PDT, and the C-alginate particles could effectively accumulate and diffuse in tumor multicellular spheres. In vitro and in vivo studies on the effects of selenium-enriched PCs on PDT in hepatocellular carcinoma showed that selenium-enriched PCs could migrate from lysosomes to mitochondria in a time-dependent manner, and that selenium-enriched PCs could induce the death of tumor cells through the generation of free radicals in vivo, increase the activities of antioxidant enzymes in vivo, induce mitochondria-mediated apoptosis, and inhibit autophagy, thus offering a relatively safe pathway to tumor treatment and showing new development perspectives [4]. It can provide a relatively safe way to treat tumors and shows a new development prospect [4].

Lin et al. [25] combined C-phycocyanin with single-walled carbon nanohorns and prepared phycocyanin-functionalized single-walled carbon nanohorn hybrids, which enhanced the photostability of C-phycocyanin and protected the single-walled carbon nanohorns from adsorption of plasma proteins, and synergistically used with PDT and photothermal therapy (PTT) to treat tumors. C-phycocyanin covalently coupled with biosilica and PDT or non-covalently coupled with indocyanine green and PTT on tumor-associated macrophages can also increase the apoptosis rate of tumor cells [26-27]. The development of PDT and PTT synergistic methods for the treatment of cancer has broadened the application of C-PC and enhanced its value in the treatment of hepatocellular carcinoma.

In addition, C-phycocyanin can inhibit the expression of multidrug-resistant genes in HepG2 cells through NF-κB and activated protein-1 (AP-1)-mediated pathways, and C-phycocyanin increases the accumulation of adriamycin in HepG2 cells in a dose-dependent manner, which results in a 5-fold increase in the susceptibility of cells to adriamycin [28]. Even in adriamycin-resistant HepG2 cells, C-PC induced the activation of apoptotic pathways such as cytochrome C and caspase-3 [29], and the results of Prabakaran et al. [30] also confirmed the inhibitory effect of C-PC on the proliferation of HepG2 cells, mediated by the inactivation of BCR-ABL signaling and the downstream PI3K/Akt pathway. mediated by BCR-ABL signaling and inactivation of downstream PI3K/Akt pathway. In addition, C-phycocyanin modifies the mitochondrial membrane potential and promotes apoptosis in cancer cells [30]. Currently, C-phycocyanin is a synergistic molecule with other drugs that have been widely used in the treatment of cancer [31]. The above studies demonstrate that C-phycocyanin has good therapeutic potential in the field of hepatocellular carcinoma.

5 Amelioration of metabolic syndrome and non-alcoholic fatty liver disease by C-phycocyanin

It has been found that C-alginin can reduce ALT and AST levels, decrease ROS production and NF-κB activation, and attenuate hepatic fibrosis in rats induced by high-fat choline-deficient diets, and thus C-alginin has a protective effect on NAFLD rats through anti-inflammatory and antioxidant mechanisms [15].

Another study on the effects of aqueous extract of Spirulina (mainly C-alginin) on NAFLD induced by a high-calorie/high-fat Western diet in C57Bl/6J mice showed that aqueous extract of Spirulina significantly improved glucose tolerance, lowered plasma cholesterol, and increased ursodeoxycholic acid in bile in mice [32]. Kaspi-Chadli et al. Kasbi-Chadli et al. [33] showed that aqueous extract of Spirulina could reduce cholesterol and sphingolipid levels in the liver and aortic cholesterol levels in hamsters fed a high-fat diet by significantly decreasing the expression of hydroxy-3-methylglutaryl-coenzyme A reductase (HMG CoA) gene, a limiting enzyme for cholesterol synthesis, and TGF-β1 gene, and that ursodeoxycholic acid levels in the feces of hamsters fed high-fat diets were increased in the high Spirulina aqueous extract treatment group.

A daily dose of C-alginin-enriched Spirulina can reduce the harmful effects of oxidative stress induced by a diet rich in lipid peroxides [34]. Ma et al. [35] found that C-alginin promoted the phosphorylation of hepatocyte AMP-dependent protein kinase (AMPK) in vivo and ex vivo, and increased the phosphorylation of acetyl coenzyme A carboxylase. In the treatment of NAFLD in mice, C-alginin can improve liver inflammation by up-regulating the expression of phosphorylated AMPK and AMPK-regulated transcription factor peroxisome proliferator-activated receptor α (PPAR-α) and its target gene, CPT1, and by down-regulating the expression of pro-inflammatory factors such as TNF-α and CD36 [35]. This suggests that C-phycocyanin can also improve lipid deposition in the liver through the AMPK pathway.

Endothelial dysfunction is associated with hypertension, atherosclerosis and metabolic syndrome. Studies in animal models of spontaneous hypertension have shown that long-term administration of C-alginin may improve systemic blood pressure in rats by increasing aortic endothelial nitric oxide synthase levels, with a dose-dependent decrease in blood pressure, and thus C-alginin may be useful in preventing endothelial dysfunction-related diseases in the metabolic syndrome [36]. In the offspring of ApoE-deficient mice fed C-alginate during gestation and lactation, male littermates had an elevated hepatic reduced/oxidized glutathione ratio and significantly lower hepatic SOD and glutathione peroxidase gene expression.

C-PC is effective in preventing atherosclerosis in adult hereditary hypercholesterolemic mice [37]. In vitro, C-phycocyanin also improved glucose production and expression of phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G-6-Pase) in high-glucose-induced insulin-resistant HepG2 cells [38]. C-alginin also increases glucose uptake in high glucose-induced insulin-resistant HepG2 cells through the insulin receptor substrate (IRS)/PI3K/Akt and Sirtuin-1 (SIRT1)/liver kinase B1 (LKB1)/AMPK signaling pathways, activates glycogen synthase, and increases the amount of glycogen [38]. C-phycocyanin can improve blood glucose and fasting serum insulin levels in tetracycline-induced diabetic mice [39]. Therefore, C-phycocyanin can maintain cellular glucose homeostasis by improving insulin resistance in hepatocytes.

6 Hepatoprotective role of C-phycocyanin in other liver diseases

Studies have shown that C-alginin can inhibit total serum cholesterol, triacylglycerol, LDL, ALT, AST, and malondialdehyde levels in mice modeled with alcoholic liver injury, significantly increase SOD levels in the liver, and promote the activation and proliferation of CD4+ T cells, which can have an ameliorative effect on alcoholic liver injury [40]. In addition, C-phycocyanin may enhance the intestinal barrier function, regulate the intestinal flora, reduce the translocation of bacteria and metabolites to the liver, and inhibit the activity of the Toll-like receptor 4 (TLR4)/NF-κB pathway, which may reduce the inflammation of the liver and prevent the occurrence of hepatic fibrosis in mice [41]. In mice with X-ray radiation-induced liver injury, C-phycocyanin can reduce radiation-induced DNA damage and oxidative stress injury by up-regulating the expression of nuclear factor (NF)-E2-related factor 2 (Nrf2) and downstream genes, such as HO-1, and play a hepatoprotective role by enhancing the activities of SOD and glutathione peroxidase [42].

7 Outlook

Liver fibrosis is the common final process of chronic liver diseases, and there is no effective therapeutic drug at present. Although some research progress has been made in the field of traditional Chinese medicine (TCM) on the reversal of liver fibrosis [43], its toxicological effects have not yet been clarified. Although the incidence of viral hepatitis has gradually decreased with the development and popularization of vaccines and antiviral drugs, the incidence of drug-induced liver injury (DILI) and liver diseases such as NAFLD has been increasing year by year with the improvement of people's living conditions [44]. Therefore, there is an urgent need to find drugs or nutrients that can help maintain normal hepatocyte function and effectively inhibit liver inflammation and fibrosis. C-alginin, with its anti-inflammatory, antioxidant, and antitumor effects, as well as good food coloring, has a wide range of applications in both the pharmaceutical and food industries.

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[20] REMIREZ D, FERNÁNDEZ V, TAPIA G, et al. Influence of C- phycocyanin on hepatocellular parameters related to liver oxidative stress and kupffer cell functioning[J]. Inflamm Res, 2002, 51(7): 351-356. doi: 10. 1007/pl00000314.

[21] TONG F, TANG X, LIU D. Phycocyanin/PEG-b-(PG-g-PEI) attenuated hepatic ischemia/reperfusion-induced pancreatic islet injury and enlarged islet functionality [J]. Int J Nanomedicine, 2019, 14: 339-351. doi: 10.2147/IJN.S190938.

［22］KUNTE M, DESAI K. The inhibitory effect of C-phycocyanin containing protein extract on human matrix metalloproteinases (MMP-2) and MMP-9 in hepatocellular cancer cell line (HepG2)［J］. and MMP-9) in hepatocellular cancer cell line (HepG2) [J].  Protein J, 2017, 36(3): 186-195. doi: 10. 1007/s10930-017-9707-0.

［23］WANG C Y, WANG X, WANG Y, et al. Photosensitization of phycocyanin extracted from microcystis in human hepatocellular carcinoma cells: implication of mitochondria-dependent apoptosis ［J］. J Photochem Photobiol B, 2012, 117: 70-79. doi: 10. 1016/j.  jphotobiol.2012.09.001.

［24］LIU X, DU J, XIE Z, et al. Lactobionic acid-modified phycocyanin nanoparticles loaded with doxorubicin for synergistic chemo- photodynamic therapy［J］. therapy[J]. Int J Biol Macromol, 2021, 186: 206- 217. doi: 10. 1016/j.ijbiomac.2021.07.047.

［25］LIN Z, JIANG B P, LIANG J, et al. Phycocyanin functionalized single-walled carbon nanohorns hybrid for near-infrared light- mediated cancer phototheranostics [J].  Carbon, 2019, 143: 814- 827. doi: 10. 1016/j.carbon.2018.12.011.

[26] PU Y, WEI M, WITKOWSKI A, et al. A hybrid biomaterial of biosilica and C-phycocyanin for enhanced photodynamic effect  towards tumor cells[J]. Biochem Biophys Res Commun, 2020, 533 (3): 573-579. doi: 10. 1016/j.bbrc.2020.09.049.

[27] WAN D H, MA X Y, LIN C, et al. Noncovalent indocyanine green conjugate of C-phycocyanin: preparation and tumor-associated macrophages-targeted photothermal therapeutics[J].   Bioconjug Chem, 2020, 31(5): 1438-1448. doi: 10. 1021/acs. bioconjchem. 0c00139.

［28］NISHANTH R P, RAMAKRISHNA B S, JYOTSNA R G, et al. C- phycocyanin inhibits MDR1 through reactive oxygen species and cyclooxygenase-2 mediated pathways in human hepatocellular carcinoma cell line[J]. Eur J Pharmacol, 2010, 649(1/3):74-83. doi: 10. 1016/j.ejphar.2010.09.011.

[29] ROY K R, ARUNASREE K M, REDDY N P, et al. Alteration of mitochondrial membrane potential by spirulina platensis C- phycocyanin induces apoptosis in the doxorubicinresistant human hepatocellular-carcinoma cell line HepG2[J].  Biotechnol Appl Biochem, 2007, 47 (Pt 3): 159-167. doi: 10. 1042/BA20060206.

[30] PRABAKARAN G, SAMPATHKUMAR P, KAVISRI M, et al. Extraction and characterization of phycocyanin from spirulina platensis and evaluation of its anticancer , antidiabetic and antiinflammatory effect[J]. Int J Biol Macromol, 2020, 153: 256- 263. doi: 10. 1016/j.ijbiomac.2020.03.009.

[31] SILVA M R O B D, M DA SILVA G, SILVA A L F D, et al. Bioactive compounds of Arthrospira spp. (spirulina) with potential anticancer activities: a systematic review[J].  ACS Chem Biol, 2021, 16 (11): 2057-2067. doi: 10. 1021/acschembio.1c00568.

[32] COUÉ M, TESSE A, FALEWÉE J, et al. Spirulina liquid extract protects against fibrosis related to non-alcoholic steatohepatitis and increases ursodeoxycholic acid [J]. Nutrients, 2019, 11 (1): 194. doi:10.3390/nu11010194.

[33] KASBI-CHADLI F, COUÉ M, AGUESSE A, et al. Spirulina liquid extract prevents metabolic disturbances and improves liver sphingolipids profile in hamster fed a high-fat diet[J]. Eur J Nutr, 2021, 60(8):4483-4494. doi: 10. 1007/s00394-021-02589-x.

[34] OULD AMARA-LEFFAD L, RAMDANE H, NEKHOUL K, et al. Spirulina effect on modulation of toxins provided by food, impact on hepatic and renal functions [J] . . Arch Physiol Biochem, 2019, 125 (2): 184-194. doi: 10. 1080/13813455.2018.1444059.

[35] MA P, HUANG R, JIANG J, et al. Potential use of C-phycocyanin in non-alcoholic fatty liver disease [J].  Biochem Biophys Res Commun, 2020, 526(4):906-912. doi: 10. 1016/j.bbrc.2020.04.001.

［36］ICHIMURA M, KATO S, TSUNEYAMA K, et al. Phycocyanin prevents hypertension and low serum adiponectin level in a rat model of metabolic syndrome［J］. Nutr Res, 2013, 33(5): 397-405. doi: 10. 1016/j.nutres.2013.03.006.

[37] COUÉ M, CROYAL M, HABIB M, et al. Perinatal administration of C-phycocyanin protects against atherosclerosis in apoE-deficient mice by modulating cholesterol and trimethylamine-N-oxide metabolisms[J]. Arterioscler Thromb Vasc Biol, 2021, 41(12): e512-e523. doi: 10. 1161/ATVBAHA.121.316848.

［38］REN Z, XIE Z, CAO D, et al. C-phycocyanin inhibits hepatic gluconeogenesis and increases glycogen synthesis via activating Akt and AMPK in insulin resistant hepatocytes [J]. Food Funct, 2018, 9(5): 2829-2839. doi: 10. 1039/c8fo00257f.

［39］OU Y, REN Z, WANG J, et al. Phycocyanin ameliorates alloxan- induced diabetes mellitus in mice ：involved in insulin signaling pathway and GK expression [J]. Chem Biol Interact, 2016, 247: 49- 54. doi: 10. 1016/j.cbi.2016.01.018.

[40] XIA D, LIU B, XIN W, et al. Protective effects of C-phycocyanin on alcohol-induced subacute liver injury in mice [J].  Journal of Applied Phycology, 2015, 28(2):765-772. doi: 10. 1007/s10811- 015-0677-3.

[41] XIE Y, LI W, ZHU L, et al. Effects of phycocyanin in modulating  the intestinal microbiota of mice [J].  Microbiologyopen, 2019, 8 (9): e00825. doi: 10. 1002/mbo3.825.

［42］LIU Q, LI W, QIN S. Therapeutic effect of phycocyanin on acute liver oxidative damage caused by X-ray［J］. Biomed Pharmacother, 2020, 130: 110553. doi: 10. 1016/j.biopha.2020.110553.

［43］SONG Y N, CHEN J, CAI F F, et al. A metabolic mechanism analysis of fuzheng-huayu formula for improving liver cirrhosis with traditional chinese medicine syndromes [J]. Acta Pharmacol Sin, 2018, 39(6): 942-951. doi: 10. 1038/aps.2017.101.

［44］XIAO J, WANG F, WONG N K, et al. Global liver disease burdens and research trends : analysis from a chinese perspective［J］. J Hepatol, 2019, 71(1):212-221. doi: 10. 1016/j.jhep.2019.03.004.

#phycocyanin #cphycocyanin #phycocyaninspirulina

[nshah01801]

Mastering Medical Mastery & Disease Prevention: A Comprehensive Exploration by Nik Shah

When it comes to mastering health, understanding medical concepts that impact disease prevention and overall well-being is essential. This article delves into various pivotal topics within the field of medical mastery, with insights from various experts such as Nik Shah and his collaborators. Whether it's overcoming immunological deficiencies, understanding the mechanisms of nitric oxide in health, or mastering therapies like plasma replacement, the importance of these medical innovations cannot be overstated. Below is a collection of books and resources that offer in-depth insights on essential medical topics, each offering valuable contributions to the field.

Mastering Immunology & Overcoming NIK Deficiency

Book: Mastering Immunology & Overcoming NIK Deficiency Link: https://www.ibs.it/mastering-immunology-overcoming-nik-deficiency-libro-inglese-vari/e/9798345621387 Immunology plays a critical role in the functioning of the body’s defense mechanisms. The book Mastering Immunology & Overcoming NIK Deficiency provides a deep dive into the complexities of immune deficiencies, particularly focusing on the NIK (NF-κB-inducing kinase) pathway, which is essential for immune responses. Written by experts including Nik Shah, this work emphasizes how overcoming NIK deficiency can bolster immune resilience, helping to prevent diseases. The insights are especially valuable for those aiming to understand the intricate workings of the immune system and its vital role in preventing chronic conditions.

Mastering Nitric Oxide Antagonists: Drugs that Inhibit Nitric Oxide Synthase (NOS) to Reverse Hypotension and Septic Shock

Book: Mastering Nitric Oxide Antagonists: Drugs that Inhibit Nitric Oxide Synthase (NOS) to Reverse Hypotension and Septic Shock Link: https://www.ibs.it/mastering-nitric-oxide-antagonists-drugs-libro-inglese-vari/e/9798345993484 The role of nitric oxide in regulating vascular tone and blood pressure is critical, and inhibiting its synthesis can be beneficial in certain medical scenarios like septic shock and hypotension. This book explores the scientific background and therapeutic implications of nitric oxide synthase inhibitors (NOS inhibitors). Authored by various researchers, including Nik Shah, this book provides a comprehensive understanding of how these antagonists work to reverse conditions that arise due to excessive vasodilation, offering new hope for clinical practices treating these life-threatening conditions.

Mastering Plasma Replacement Therapy

Book: Mastering Plasma Replacement Therapy Link: https://www.ibs.it/mastering-plasma-replacement-therapy-libro-inglese-vari/e/9798345873175 Plasma replacement therapy is one of the frontiers of regenerative medicine and trauma care. In Mastering Plasma Replacement Therapy, the authors provide a detailed analysis of the use of synthetic and donor plasma for patients undergoing critical conditions like burns or hemorrhages. The book discusses the mechanisms behind plasma volume restoration and its vital role in improving patient outcomes. Written by Nik Shah and his collaborators, this book offers an expert perspective on how plasma therapy can be optimized in clinical settings.

Mastering Prostate Cancer: Empowering Your Journey to Health and Healing

Book: Mastering Prostate Cancer: Empowering Your Journey to Health and Healing Link: https://www.ibs.it/mastering-prostate-cancer-empowering-your-libro-inglese-vari/e/9798303224353 Prostate cancer is one of the most common cancers affecting men. Mastering Prostate Cancer is an empowering guide that offers not just clinical insights but also motivational advice for patients embarking on their journey to health and healing. Nik Shah, alongside other experts, provides a thorough exploration of the treatment modalities, lifestyle changes, and psychological support necessary for navigating this challenging diagnosis. This book is a comprehensive resource for anyone looking to understand prostate cancer in its various stages and treatment options.

Mastering Radiotherapy and Chemotherapy

Book: Mastering Radiotherapy and Chemotherapy Link: https://www.ibs.it/mastering-radiotherapy-chemotherapy-libro-inglese-vari/e/9798345581353 Cancer treatments such as radiotherapy and chemotherapy are well-known, yet their application and advancements in clinical practice require a thorough understanding. Mastering Radiotherapy and Chemotherapy offers an in-depth look at these therapies, highlighting new techniques, drug combinations, and patient management strategies. Written by Nik Shah and other specialists, this book serves as an essential guide for medical professionals and patients alike, offering insights into the evolving landscape of cancer treatment.

Mastering Red Blood Cells: The Science of Oxygen Transport and Cellular Health

Book: Mastering Red Blood Cells: The Science of Oxygen Transport and Cellular Health Link: https://www.ibs.it/mastering-red-blood-cells-science-libro-inglese-vari/e/9798303312142 Red blood cells are crucial for oxygen transport and maintaining cellular health. This book delves into the science behind red blood cells, exploring their role in oxygen delivery and how disorders related to red blood cells, such as anemia, can impact overall health. The authors, including Nik Shah, bring a detailed scientific approach to this topic, offering vital information for both healthcare professionals and individuals interested in improving their health through understanding the mechanisms that keep red blood cells functioning optimally.

Mastering the Sciatic Nerve

Book: Mastering the Sciatic Nerve Link: https://www.ibs.it/mastering-sciatic-nerve-libro-inglese-vari/e/9798303018426 Sciatic nerve pain is a common ailment that affects millions of people worldwide. In Mastering the Sciatic Nerve, readers are introduced to both the anatomical structure of the sciatic nerve and various treatment strategies to manage sciatica. Nik Shah and his co-authors provide clear and actionable insights into how individuals can prevent and treat sciatic nerve pain, offering medical mastery for improving the quality of life for those suffering from this condition.

Mastering Tissue Functioning: Understanding the Science, Healing, and Regeneration of Human Tissues

Book: Mastering Tissue Functioning: Understanding the Science, Healing, and Regeneration of Human Tissues Link: https://www.ibs.it/mastering-tissue-functioning-understanding-science-libro-inglese-vari/e/9798303647367 Understanding how tissues regenerate and heal is fundamental in medical science. Mastering Tissue Functioning offers a detailed examination of the processes involved in tissue regeneration, including stem cell therapies, tissue engineering, and wound healing. The book is authored by Nik Shah and other medical experts, providing readers with an invaluable resource to explore cutting-edge treatments and advancements in tissue repair.

Mastering Vasopressin Agonists: A Comprehensive Guide to Mechanisms, Applications, and Innovations

Book: Mastering Vasopressin Agonists: A Comprehensive Guide to Mechanisms, Applications, and Innovations Link: https://www.ibs.it/mastering-vasopressin-agonists-comprehensive-guide-libro-inglese-vari/e/9798300424527 Vasopressin, a hormone that plays a crucial role in regulating blood pressure and water retention, has therapeutic applications in various clinical settings. This book explores the mechanisms of vasopressin agonists, their clinical use in managing conditions such as septic shock, and innovations in their development. Nik Shah and other researchers contribute their expertise, offering a complete guide to these potent therapeutic agents.

Transforming Growth Factor Beta (TGF-β) Receptors: A Comprehensive Exploration of Their Role in Cell Biology, Disease, and Therapeutics

Book: Transforming Growth Factor Beta (TGF-β) Receptors: A Comprehensive Exploration of Their Role in Cell Biology, Disease, and Therapeutics Link: https://www.ibs.it/transforming-growth-factor-beta-tgf-libro-inglese-vari/e/9798303016064 Growth factors, particularly TGF-β, have been identified as key players in cell signaling, disease progression, and therapeutic strategies. This book provides an in-depth exploration of TGF-β receptors, offering new perspectives on their involvement in cancer, fibrosis, and other diseases. Nik Shah’s work alongside other leading scientists presents comprehensive insights into how these receptors can be targeted for therapeutic purposes, making it a vital resource for advancing medical research and treatment approaches.

By exploring these advanced topics and books, readers gain a well-rounded understanding of disease prevention, therapeutic advancements, and cutting-edge medical treatments, all underpinned by the expertise of Nik Shah and his collaborators. These resources empower readers with knowledge to enhance their health, prevent diseases, and stay informed on the latest medical breakthroughs.

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@nshah01801

[kingherbs]

Chemical properties & pharmacological effects of Neferine

Abstract

Neferine is a natural bisbenzylisoquinoline alkaloid, mainly extracted from plants of the Nelumbo family (such as lotus seed embryo). In recent years, its wide range of biological activities (such as cardiovascular protection, anti-tumor, antioxidant, etc.) has attracted the attention of researchers. This paper reviews its chemical structure, pharmacological mechanism and potential applications, and looks forward to future research directions.

1. Introduction

Neferine has a long history in traditional medicine. Lotus seed heart (embryo) is recorded in the Compendium of Materia Medica as a medicinal material for clearing heat, calming the nerves and lowering blood pressure. As one of the main active ingredients of lotus seed heart, neferine exhibits diverse biological activities due to its unique bisbenzylisoquinoline structure. With the rise of natural product research, the pharmacological potential of neferine has gradually been revealed.

2. Chemical properties

Methyl neferine (C₃₈H₄₄N₂O₆, CAS number: 2292-16-2) belongs to the bis-benzylisoquinoline alkaloids, which are composed of two benzylisoquinoline units connected by ether bonds (Figure 1). It has a large molecular weight (624.77 g/mol) and high lipid solubility. It can be separated and purified from lotus seed germ by high performance liquid chromatography (HPLC) or mass spectrometry.

3. Pharmacological effects and mechanisms

3.1 Cardiovascular system protection

1. Anti-arrhythmic: By inhibiting the L-type calcium channel (LTCC) and delayed rectifier potassium channel (IK) of myocardial cells, it regulates the action potential duration and reduces the risk of arrhythmia.

2. Anti-hypertension and vasodilation: It activates the nitric oxide (NO) signaling pathway, promotes the release of NO by endothelial cells, and leads to relaxation of vascular smooth muscle.

3. Anti-thrombosis: Inhibits platelet aggregation induced by platelet activating factor (PAF) and reduces the risk of thrombosis.

3.2 Antioxidant and anti-inflammatory

- Scavenges free radicals: Neutralizes reactive oxygen species (ROS) through phenolic hydroxyl structure and reduces oxidative stress damage.

- Inhibits inflammatory factors: Downregulates NF-κB pathway, reduces the release of pro-inflammatory factors such as TNF-α and IL-6, and shows protective effects in acute lung injury models.

3.3 Anti-tumor activity

- Induce apoptosis: Activates mitochondrial apoptosis pathway (such as Bax/Bcl-2 imbalance, caspase-3 activation), inhibits breast cancer MCF-7 cell proliferation.

- Inhibits metastasis: Inhibits lung cancer A549 cell invasion and migration by blocking PI3K/Akt/mTOR pathway.

3.4 Neuroprotective effect

- Anti-Alzheimer's disease (AD): Reduce β-amyloid protein (Aβ) deposition, inhibit tau protein hyperphosphorylation, and improve cognitive dysfunction in mice.

4. Applications and challenges

4.1 Traditional and modern applications

- Traditional Chinese medicine uses: Lotus seeds are used to make tea to reduce internal heat and calm the nerves.

- Modern drug development: As a lead compound, explore the application of its derivatives in anti-tumor or cardiovascular diseases.

4.2 Safety and limitations

- Toxicity: Animal experiments show low acute toxicity (LD₅₀ > 2 g/kg), but long-term use may affect liver and kidney function.

- Bioavailability: High lipid solubility but poor water solubility, and the absorption rate needs to be improved through nanoformulation or structural modification.

5. Future research directions

1. Clinical transformation: Promote clinical trials to verify its efficacy on human diseases (such as hypertension and cancer).

2. Structural optimization: Enhance targeting and reduce side effects through chemical modification.

3. Multi-omics research: Combine metabolomics and proteomics to analyze its multi-target mechanism of action.

6. Conclusion

As a natural active molecule, neferine has multi-target and multi-pathway pharmacological properties and has significant potential in the treatment of cardiovascular diseases, tumors and neurodegenerative diseases. In the future, it is necessary to strengthen the connection between basic and clinical research and promote its application from laboratory to clinical application.

References ：

1. Deng Y, et al. *Neferine inhibits colorectal cancer cell growth through ROS-mediated PI3K/Akt pathway*. Cancer Lett. 2019.

Liu CM, et al. *Neferine induces apoptosis by modulating Bcl-2 family proteins in human breast cancer cells*. Phytomedicine. 2020.

3. Chinese Pharmacopoeia Commission. *Pharmacopoeia of the People’s Republic of China*. 2020 Edition. article from:Chemical properties & pharmacological effects of Neferine - Kingherbs

[alvavi]

Does What We Eat Fuel Cancer? Unveiling the Startling Link Between Diet and Tumor Growth

In an era where global cancer rates are rising alarmingly — 19.3 million new cases annually , according to the World Health Organization (WHO) — scientists are increasingly investigating how everyday dietary choices may inadvertently nourish malignant cells. By 2040, these numbers are projected to surge by 50%, prompting urgent questions: Could our meals be silent accomplices in cancer proliferation? Let’s explore the science behind this critical connection.

1. Processed Foods: The Hidden Cancer Accelerators

Processed and ultra-processed foods dominate modern diets, but their impact extends beyond convenience. A landmark 2022 study in JAMA Oncology linked high consumption of processed meats (e.g., bacon, sausages) and refined sugars to a 20% increased risk of colorectal, breast, and pancreatic cancers.

Nitrosamines in Processed Meats : Compounds like sodium nitrite, used to preserve meats, convert into carcinogenic nitrosamines in the body. These damage DNA and disrupt cellular repair mechanisms. The International Agency for Research on Cancer (IARC) classifies processed meats as Group 1 carcinogens , alongside tobacco.

Sugar and Insulin Spikes : Refined sugars trigger insulin surges, which activate IGF-1 pathways — a known driver of tumor growth. A 2023 study in Nature Reviews Cancer highlighted that high-glycemic diets correlate with aggressive breast cancer subtypes.

2. Antioxidants: Nature’s Shield Against Cellular Damage

While some foods harm, others heal. Antioxidant-rich diets combat oxidative stress, a key factor in cancer development. Research from Harvard T.H. Chan School of Public Health reveals that diets high in fruits, vegetables, and whole grains reduce cancer risk by 30–40% .

Key Antioxidant Sources :

Berries : Packed with anthocyanins, which inhibit tumor angiogenesis (blood vessel formation).

Turmeric : Curcumin, its active compound, suppresses NF-κB, a protein linked to inflammation and metastasis.

Green Tea : Epigallocatechin gallate (EGCG) induces apoptosis (cell death) in cancer cells.

3. Obesity: The Overlooked Bridge Between Diet and Cancer

Excess body weight contributes to 13 cancer types , including endometrial, kidney, and esophageal cancers. The American Institute for Cancer Research (AICR) attributes 40% of U.S. cancer cases to obesity-related factors.

Mechanisms :

Chronic Inflammation : Fat tissue releases pro-inflammatory cytokines, fostering a microenvironment where tumors thrive.

Hormonal Imbalances : Obesity elevates estrogen levels, promoting hormone-sensitive cancers like breast and ovarian.

Example : Postmenopausal women with a BMI >30 have a 20–40% higher risk of breast cancer than those with a BMI <25

4. Practical Dietary Strategies for Cancer Prevention

Adopting a whole-foods-based diet can significantly lower cancer risk. Here’s how:

Limit Processed Foods : Replace deli meats with plant-based proteins (e.g., lentils, tofu).

Prioritize Fiber : Aim for 25–30g daily from oats, beans, and vegetables to support gut health.

Embrace Healthy Fats : Swap trans fats for omega-3-rich foods (e.g., salmon, walnuts), which reduce inflammation.

Moderate Sugar Intake : Opt for natural sweeteners like dates and avoid sugary beverages.

5. Emerging Research: The Microbiome Connection

The gut microbiome plays a pivotal role in immune regulation. A 2024 study in Cell found that high-fiber diets promote beneficial bacteria like Lactobacillus , which enhance immunotherapy efficacy in melanoma patients. Conversely, low microbiome diversity is linked to colorectal cancer progression.

Conclusion: Your Plate, Your Power

Cancer is not inevitable. While genetics load the gun, lifestyle — especially diet — pulls the trigger. By prioritizing nutrient-dense foods and minimizing carcinogens, we can reshape our biological terrain. As Dr. William Li, author of Eat to Beat Disease , states: “Food is medicine. What we choose to eat today writes the story of our health tomorrow.”

Call to Action : Start small — swap a sugary snack for a handful of nuts, or add a serving of greens to your lunch. Every bite is a choice: Will it nourish or endanger?

[blueoaknx]

Mitochondria Combat Chronic Inflammation

Introduction

Chronic inflammation is a pathophysiological condition linked to numerous diseases, including obesity, diabetes, cardiovascular diseases, and neurodegenerative disorders. Mitochondria, the cellular powerhouses, are pivotal not only for ATP production but also for regulating cellular metabolism, redox balance, and apoptosis. Recent studies reveal that mitochondria play a crucial role in modulating inflammatory responses, and their dysfunction is often implicated in chronic inflammatory states. This article explores the intricate mechanisms by which mitochondria influence chronic inflammation and their potential as therapeutic targets.

Mitochondrial Structure and Function

Mitochondria possess a double-membrane structure that includes:

Outer Membrane: Contains porins that allow the passage of small molecules.

Inner Membrane: Rich in cardiolipin and contains the electron transport chain (ETC) complexes crucial for oxidative phosphorylation.

Matrix: Contains enzymes for the tricarboxylic acid (TCA) cycle, mitochondrial DNA (mtDNA), and ribosomes.

These structural features enable mitochondria to perform several essential functions, including ATP synthesis, calcium buffering, and reactive oxygen species (ROS) regulation.

Mitochondrial Dysfunction and Chronic Inflammation

Mitochondrial dysfunction is characterized by reduced ATP production, increased ROS generation, and impaired metabolic signaling. Key contributors to mitochondrial dysfunction include:

Oxidative Stress: Excessive ROS can damage mitochondrial components, leading to a vicious cycle of increased inflammation.

Aging: Aging is associated with mitochondrial dysfunction, contributing to the onset of chronic inflammatory diseases.

Environmental Toxins: Exposure to pollutants and toxins can induce mitochondrial damage.

Mitochondrial dysfunction is implicated in the activation of pro-inflammatory pathways, including:

NLRP3 Inflammasome Activation: Mitochondrial ROS and mtDNA release can activate the NLRP3 inflammasome, leading to the maturation and secretion of pro-inflammatory cytokines such as IL-1β and IL-18.

NF-κB Pathway: Mitochondrial stress can activate the NF-κB signaling pathway, promoting the expression of pro-inflammatory genes.

Mechanisms by Which Mitochondria Combat Chronic Inflammation

Energy Homeostasis and Immune Cell Function

Mitochondria are essential for the bioenergetic demands of immune cells, particularly during inflammatory responses. Immune cells like macrophages and T-cells switch from oxidative phosphorylation to glycolysis during activation, a process known as the Warburg effect. Mitochondria facilitate this metabolic flexibility by:

Providing substrates for glycolysis and subsequent oxidative phosphorylation.

Regulating ATP levels to support energy-intensive processes, such as cytokine production and phagocytosis.

Regulation of ROS and Redox Signaling

Mitochondria generate ROS as byproducts of the ETC. While excessive ROS can induce oxidative stress, physiological levels of ROS act as signaling molecules that modulate immune responses:

ROS can activate redox-sensitive transcription factors such as Nrf2, promoting the expression of antioxidant genes that mitigate oxidative stress.

Controlled ROS production aids in the differentiation of T-helper cells and enhances the immune response.

Apoptosis and Clearance of Damaged Cells

Mitochondria are central to the intrinsic apoptotic pathway, releasing cytochrome c and other pro-apoptotic factors that initiate caspase cascades. Effective apoptosis is crucial for:

Removing damaged or dysfunctional cells that could perpetuate inflammation.

Promoting an anti-inflammatory environment through the clearance of dead cells and debris, thereby preventing secondary necrosis and the associated inflammatory response.

Mitophagy: Mitochondrial Quality Control

Mitophagy is the selective autophagic degradation of damaged mitochondria, crucial for maintaining mitochondrial quality. Key mechanisms involved in mitophagy include:

PINK1/Parkin Pathway: PINK1 accumulates on damaged mitochondria, recruiting Parkin, which ubiquitinates mitochondrial proteins, signaling for degradation by the autophagy machinery.

Enhanced mitophagy reduces the release of pro-inflammatory factors and maintains cellular homeostasis.

Mitochondrial Biogenesis and Adaptation

Mitochondrial biogenesis is regulated by PGC-1α and other transcription factors. Increasing mitochondrial biogenesis can enhance cellular energy capacity and improve metabolic flexibility, which is particularly beneficial in inflammation. Strategies to promote mitochondrial biogenesis include:

Exercise: Physical activity enhances PGC-1α expression and mitochondrial function.

Nutritional Interventions: Certain bioactive compounds, like resveratrol and curcumin, have been shown to stimulate mitochondrial biogenesis.

Therapeutic Implications

Given their critical role in modulating inflammation, mitochondria represent promising therapeutic targets. Potential strategies include:

Nutraceuticals: Compounds like Coenzyme Q10 and α-lipoic acid may enhance mitochondrial function and reduce oxidative stress.

Exercise Interventions: Regular physical activity can improve mitochondrial health and reduce chronic inflammation.

Mitochondrial-targeted Therapies: Developing drugs that specifically target mitochondrial pathways could provide new treatment avenues for inflammatory diseases.

Conclusion

Mitochondria are integral to the regulation of chronic inflammation through their roles in energy metabolism, ROS management, apoptosis, mitophagy, and biogenesis. Understanding the complex interplay between mitochondrial function and inflammatory processes is essential for developing effective therapeutic strategies. By targeting mitochondrial health, we can potentially mitigate chronic inflammation and its associated diseases, paving the way for innovative approaches to improve public health outcomes. Continued research into mitochondrial biology will undoubtedly reveal further insights into their role in inflammation and disease.

[oxygenrn]

**Deep Analysis of Astaxanthin: Mechanisms, Benefits, and Clinical Evidence**

Astaxanthin, a potent carotenoid found in microalgae, salmon, krill, and crustaceans, has gained attention for its unique antioxidant properties and potential anti-aging benefits. Below is a comprehensive analysis of its mechanisms, clinical applications, and practical considerations.

---

### **1. Molecular Mechanisms of Action**

Astaxanthin’s efficacy stems from its molecular structure and multifaceted biological activity:

- **Antioxidant Power**:

- Astaxanthin **quenches free radicals** (ROS and RNS) 6,000x more effectively than vitamin C and 100x more than vitamin E ([*Food Chemistry*, 2011](https://www.sciencedirect.com/science/article/abs/pii/S0308814611002535)).

- Its unique **polar-nonpolar-polar structure** allows it to span cell membranes, protecting both lipid and aqueous cellular regions ([*Marine Drugs*, 2013](https://www.mdpi.com/1660-3397/11/3/706)).

- **Anti-Inflammatory Effects**:

- Inhibits NF-κB and COX-2 pathways, reducing pro-inflammatory cytokines (e.g., TNF-α, IL-6) ([*Molecular Nutrition & Food Research*, 2011](https://onlinelibrary.wiley.com/doi/10.1002/mnfr.201100230)).

- **Mitochondrial Support**:

- Enhances mitochondrial efficiency by reducing oxidative damage and improving ATP production ([*Nutrients*, 2021](https://www.mdpi.com/2072-6643/13/2/395)).

- **Cellular Senescence Modulation**:

- Reduces markers of cellular aging (e.g., p16, p21) by clearing senescent cells in preclinical models ([*Aging*, 2020](https://www.aging-us.com/article/103334/text)).

---

### **2. Clinically Validated Benefits**

#### **A. Skin Health & UV Protection**

- **Mechanism**: Neutralizes UV-induced free radicals and boosts collagen synthesis.

- **Evidence**:

- 12 mg/day for 16 weeks improved skin elasticity and reduced wrinkles in a double-blind trial ([*Acta Biochimica Polonica*, 2012](https://www.actabp.pl/pdf/3_2012/663.pdf)).

- Topical astaxanthin + oral supplementation reduced UV-induced hyperpigmentation by 40% ([*Journal of Cosmetic Dermatology*, 2018](https://onlinelibrary.wiley.com/doi/abs/10.1111/jocd.12393)).

#### **B. Eye Health**

- **Mechanism**: Crosses the blood-retinal barrier, protecting photoreceptors and reducing oxidative stress.

- **Evidence**:

- 6 mg/day for 4 weeks improved retinal blood flow and reduced eye fatigue in computer users ([*Journal of Clinical Biochemistry and Nutrition*, 2017](https://www.jstage.jst.go.jp/article/jcbn/61/1/61_17-35/_article)).

- May slow age-related macular degeneration (AMD) by reducing lipid peroxidation ([*Nutrients*, 2013](https://www.mdpi.com/2072-6643/5/3/891)).

#### **C. Exercise Performance & Recovery**

- **Mechanism**: Reduces exercise-induced oxidative stress and muscle damage.

- **Evidence**:

- 12 mg/day for 8 weeks improved cycling time-trial performance and reduced lactate buildup ([*Biology of Sport*, 2021](https://www.termedia.pl/Journal/-92/FullText-58203)).

- Accelerated recovery in athletes by lowering CRP and creatine kinase levels ([*International Journal of Sports Medicine*, 2011](https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0031-1275641)).

#### **D. Cognitive Function**

- **Mechanism**: Crosses the blood-brain barrier, reducing neuroinflammation and amyloid-beta toxicity.

- **Evidence**:

- 12 mg/day for 12 weeks improved memory and attention in middle-aged adults with age-related cognitive decline ([*Journal of Clinical Biochemistry and Nutrition*, 2012](https://www.jstage.jst.go.jp/article/jcbn/51/2/51_12-32/_article)).

- Animal studies show protection against Alzheimer’s pathology ([*Marine Drugs*, 2018](https://www.mdpi.com/1660-3397/16/4/147)).

#### **E. Cardiovascular Health**

- **Mechanism**: Improves lipid profiles, reduces arterial stiffness, and enhances endothelial function.

- **Evidence**:

- 12–18 mg/day lowered LDL oxidation and increased HDL in hyperlipidemic patients ([*Atherosclerosis*, 2010](https://www.atherosclerosis-journal.com/article/S0021-9150(09)00660-5/fulltext)).

- Reduced arterial plaque formation in ApoE-deficient mice ([*Biochemical and Biophysical Research Communications*, 2010](https://www.sciencedirect.com/science/article/abs/pii/S0006291X10008127)).

---

### **3. Safety & Bioavailability**

- **Dosage**:

- **4–12 mg/day** is well-tolerated in clinical trials. Higher doses (up to 40 mg) showed no toxicity but may cause orange-red skin pigmentation.

- **Bioavailability**:

- Fat-soluble; pair with dietary fats (e.g., fish oil, avocado) for optimal absorption.

- **Natural vs. Synthetic**: Natural astaxanthin (from *Haematococcus pluvialis*) has 20x higher antioxidant activity than synthetic forms ([*Journal of Agricultural and Food Chemistry*, 2004](https://pubs.acs.org/doi/10.1021/jf049124j)).

- **Side Effects**:

- Rare and mild (e.g., stomach upset). No drug interactions reported, but caution with anticoagulants due to theoretical antiplatelet effects.

---

### **4. Comparison to Other Antioxidants**

| **Feature** | **Astaxanthin** | **Vitamin C** | **CoQ10** |

|---------------------------|--------------------------|---------------------|---------------------|

| **Antioxidant Strength** | 6,000x Vitamin C | Moderate | Moderate |

| **Membrane Penetration** | Both lipid & aqueous | Aqueous only | Lipid only |

| **Bioavailability** | Enhanced with fats | Water-soluble | Requires fats |

| **Unique Benefits** | Skin, eyes, mitochondria| Collagen synthesis | Mitochondrial energy|

---

### **5. Limitations & Research Gaps**

- **Human Trials**: Most studies are small or short-term (4–24 weeks). Long-term effects (>1 year) are understudied.

- **Dose-Response**: Optimal dosing for specific conditions (e.g., cognitive decline) remains unclear.

- **Synergy**: Limited data on combining astaxanthin with other antioxidants (e.g., vitamin E, selenium).

---

### **6. Practical Recommendations**

- **For Skin & Anti-Aging**: 6–12 mg/day + topical serums (0.1–2% astaxanthin).

- **For Exercise Recovery**: 12 mg pre-workout.

- **For Brain Health**: Pair with omega-3s (DHA/EPA) to enhance neuroprotection.

- **Source**: Choose **natural astaxanthin** (e.g., *Haematococcus pluvialis* extracts) over synthetic versions.

---

### **Conclusion**

Astaxanthin is a uniquely versatile antioxidant with robust preclinical and emerging clinical evidence for skin health, cognitive function, exercise performance, and anti-aging. While not a “miracle cure,” it complements a holistic strategy of diet, exercise, and stress management. Always consult a healthcare provider before starting supplementation, especially if pregnant or on medications.

**Key Takeaway**: Astaxanthin’s ability to protect multiple cellular compartments and modulate inflammation makes it a standout candidate for mitigating age-related decline.

[blackbiobiotech]

Understanding ROS1 and MYD88 Mutations: Key Diagnostic Tools for Oncologists

Cancer research and treatment are rapidly evolving, with molecular diagnostics playing a pivotal role in shaping personalized treatment plans. With advances in genetic testing, clinicians can identify specific mutations that drive the development of various cancers, allowing for more targeted therapies. Among the most important genetic markers in cancer diagnostics are ROS1 and MYD88 mutations. These mutations are linked to specific cancers, including non-small cell lung cancer (NSCLC) and certain lymphomas. 3B BlackBio Biotech offers cutting-edge solutions for detecting these mutations, including the ROS1 PCR Kit and MYD88 Mutation Detection Kit. These kits help clinicians make informed decisions based on precise genetic data.

ROS1 PCR Kit: Unveiling Key Insights for Lung Cancer Treatment

ROS1 gene fusions are known to occur in a subset of non-small cell lung cancers (NSCLC). ROS1 mutations are associated with a high potential for targeted therapy, as they make tumors sensitive to certain types of tyrosine kinase inhibitors (TKIs). However, accurately detecting ROS1 gene rearrangements is critical for determining the suitability of these therapies.

3B BlackBio Biotech’s ROS1 Gene Fusions Detection Kit offers a highly sensitive and reliable method for identifying ROS1 mutations. By detecting gene fusions, this kit provides valuable diagnostic information that can directly influence treatment choices. ROS1 mutations are relatively rare, but their detection is essential for selecting the most effective therapy. This PCR-based kit uses advanced techniques to ensure accurate results, making it an essential tool for oncologists looking to personalize cancer treatments.

The ROS1 mutations kit is particularly important for NSCLC patients who may benefit from therapies like crizotinib, an FDA-approved drug that targets ROS1 gene rearrangements. The ability to identify these mutations early on ensures that patients receive the best possible care, improving their prognosis and quality of life.

MYD88 PCR Kit: A Key Player in Lymphoma Diagnostics

MYD88 mutations are commonly found in various types of lymphoma, particularly in Waldenström macroglobulinemia (WM), a rare and slow-growing cancer of the blood. MYD88 mutations are crucial for diagnosing and predicting the course of the disease, as well as determining the most effective treatment options. The detection of MYD88 mutations allows for a more precise diagnosis and a tailored approach to treatment.

The MYD88 Mutation Detection Kit provides a powerful tool for identifying MYD88 mutations in patients with suspected lymphoma. This PCR-based test detects mutations in the MYD88 gene, which are linked to abnormal activation of the NF-κB pathway—a key factor in the development of lymphoma. Accurate detection of MYD88 mutations helps clinicians understand the molecular profile of the tumor, allowing them to choose the most appropriate treatment for the patient.

The MYD88 PCR kit is not only useful for diagnosing Waldenström macroglobulinemia but also for assessing other lymphoma subtypes. With its high sensitivity and precision, this kit plays a crucial role in the clinical management of lymphoma patients, improving diagnostic accuracy and treatment outcomes.

The Role of 3B BlackBio Biotech in Advancing Cancer Diagnostics

3B BlackBio Biotech has been at the forefront of providing high-quality diagnostic kits for genetic mutations associated with various cancers. Their ROS1 PCR Kit and MYD88 Mutation Detection Kit are prime examples of the company’s commitment to enhancing precision medicine. These kits enable clinicians to detect key mutations, ensuring that patients receive the most effective treatments based on their genetic profiles.

By offering advanced tools like the ROS1 Gene Fusions Detection Kit and the MYD88 Mutation Detection Kit, 3B BlackBio Biotech is contributing significantly to the personalization of cancer care. These diagnostic solutions help oncologists make data-driven decisions, ultimately improving patient outcomes and advancing the fight against cancer.

For more information on 3B BlackBio Biotech's advanced PCR kits, visit at https://3bblackbio.com/.

[darkmaga-returns]

Story at-a-glance

Butyrate, produced by gut bacteria when they ferment dietary fiber, acts as a signaling molecule in the gut-brain axis, influencing stress, pain tolerance, immunity, and brain health

Through multiple mechanisms, including specific enzyme inhibition and NF-κB pathway regulation, butyrate reduces neuroinflammation and protects against neurodegenerative conditions like Alzheimer's and Parkinson's disease

Butyrate influences key neurotransmitters including GABA, serotonin, and dopamine, while also increasing brain-derived neurotrophic factor (BDNF), which supports neuronal growth and cognitive function

The vagus nerve serves as a communication highway between the gut and the brain, transmitting signals about butyrate levels that affect mood regulation, stress response, and immune function

Optimizing gut health through dietary fiber and homemade fermented foods helps promote butyrate production and maintain a healthy gut-brain connection

[dhakshin-ayurveda]

Piper Longum Extract: Uncovering the Ancient Healing Properties of Long Pepper

Introduction

Originally from the tropical regions of South Asia and Southeast Asia, Piper longum commonly referred to as long pepper, is a flowering vine renowned for its medicinal value in both traditional Ayurvedic and Chinese practice. Long pepper is the native to India and South East Asian countries and has been used in traditional medicines from ancient days for digestive problems, respiratory disorders and anti-inflammatory disorders. In the present time, the performance of clinical analyses points to the medicinal value of Piper Longum Extract as the extract comprises certain essential alkaloids, lignans, and other valuable bioactive constituents that play diverse roles in the overall health of the body. The article focuses on the history of Piper Longum Extract, its chemical profile and recent evidence for therapeutic uses.

1.Historical Background and Cultural Significance of Long Pepper

Long pepper is as old as many ancient civilizations as it has been widely used since prehistoric times. Fixed strongly in India, Greece and Rome it was considered very dear as spice and medicine until the arrival of black pepper. Charaka Samhita and Sushruta Samhita mention long pepper as: The conditions that can be treated with the help of long pepper are gastrointestinal problems, cough, and fever .

TCMdescribes the use of Piper longum to tone up the areas that are cold, eliminate cold and to treat pain. With the past centuries, long pepper has been used as a traditional remedy to cure many diseases ; now it remains a key component of herbal medicine in Asia .

2. Chemical Composition of Piper Longum Extract

Actually, Piper Longum Extract is a complex of active compounds: alkaloids, lignans and volatile oils, as well as amides. They include piperine, which in fact bears ninety percent of this product’s therapeutic value, piperlongumine, and piperanine. 

Piperine(C₁₇H₁₉NO₃): A bitter principle contributing to the pungent flavor and numerous physiological activities, such as promotion of nutritional uptake and reduction of inflammation .

Piperlongumine (C₁₇H₁₉NO₅): A privileged amide with demonstrable anticancer and free radical scavenging properties, piperlongumine has been recommended for its pro-apoptotic effect in cancerous cells. 

Lignans:Suchassesamin and cubebin, which has antioxidant and hepatoprotective effects and other biologically active compounds. 

EssentialOils: These oils which include myristicin and elemicin play a role in the antimicrobial and carminative properties of the extract .

3. Health Benefits of Piper Longum Extract

a) Enhanced Digestive Health and Nutrient Absorption

Piper Longum Extracts have generally been used to activate digestive enzymes and bile that are used in the digestion of foods as well as facilitating nutrient digestion. Long pepper increases gastric secretions and helps keep gastrointestinal issues, such as swelling and indigestion, at bay. 

Mechanism of Action: The two phytochemicals present in the extract include piperine and piperlongumine that enhances the concoction’s capability to stimulate digestive enzymes like amylase, proteases, and lipases. Piperine has also been established to reduce enzymes such as UDP-glucuronosyltransferase thus enhancing intake of nutrients and herbal compounds such as curcumin and beta-carotene.

b) Anti-inflammatory and Antioxidant Effects

Piper Longum Extract is potent on antioxidation and anti-inflammatory activity which are useful in combating oxidative stress and inflammation in the body system.

Anti-inflammatory Pathways: Long pepper extract compounds interfere with the NF-κB and COX-2 enzymes involved in signalling inflammation. Since Piper Longum Extract inhibits these pathways it has anti-inflammatory properties that can help manage diseases such as arthritis.

Oxidative Stress Reduction: Research has pointed out that piperlongumine and piperine boost the amounts of antioxidant enzymes like catalase and superoxide dismutase which are very important in eliminating free radicals from the cells and adding to the overall wellness of the cells.

c) Respiratory Health and Immune Support

In traditional medicine systems, Piper Longum Extract has often been turned to for respiratory disorders such as cough, asthma, and bronchitis owing to its expectorant and bronchodilator activity. 

Expectorant Action: The extract is useful in the breakdown of thickened mucous and phlegm in the respiratory system hence easy clearance. This to a great extent is advantageous if the patient has a chronic respiratory illness which may cause obstructions of the airway. 

Immune Modulation: Piper Longum proved to have an immune enhancing property which was evident by promoting the activity of macrophage as well as lymphocytes which are responsible for defensive mechanisms against infections.

d)Metabolic and Weight Management Benefits

The bioactive present in long peppers includes those associated with the functionality for appropriate metabolic appropriate lipid metabolism in management of obesity with related thermogenesis.

•Thermogenic Properties: The found alkaloids; piperine, and piperlongumine elevate the levels of thermogenesis which is the burning of calories to generate heat. This effect can help in Weight Loss and Fat loss because it will help increase the Metabolism rate.

 •Lipid Profile Improvement: Piper Longum Extract is also considered to reduce concentration of LDL Cholesterol and augment that of HDL cholesterol thus supporting the cardiovascular system.

e)Potential Anti-Cancer Properties

Among all the realizations of Piper Longum Extract, the most significant area of focus is its anti-carcinogenic properties, especially because of piperlongumine. 

Inducing Apoptosis in Cancer Cells: Piperlongumine kills the cancerous cells by the production of ROS in cancer cells while sparing normal cells leads to the apoptosis of cancer cells .

Inhibition of Angiogenesis: Piperlongumine also has an effect on the suppression of angiogenesis; a process through which tissue formation initiates new blood vessels which supply nutrients to the tumor. It also plays a major role in decelerating the growth and development of tumors

4.Mechanisms of Action in Piper Longum’s Therapeutic Effects

Piper Longum Extract’s therapeutic effects are attributed to several biological mechanisms: 

1.Enzyme Inhibition: Piper Longum Extract being an enzyme inhibitor to cytochrome P450 and UDP- glucuronosyltransferase, the other therapeutic compounds it releases is then made bioavailable. 

2.Immune System Modulation: Long pepper also includes macrophages and cytokine production of the immune system and hence improves its defense to pathogens. 

3.Oxidative Stress Reduction: Piperlongumine stimulates the formation of antioxidant enzymes and reduces levels of reactive oxygen species preventing the oxidative damage of cells

5.Modern Applications of Piper Longum Extract in Health and Wellness

In traditional medicine, Piper Longum Extract is frequently used to address respiratory issues like cough, asthma, and bronchitis due to its expectorant and bronchodilator properties.

 Expectorant Action: The extract helps in loosening mucus and phlegm in the respiratory tract, making it easier to expel. This effect is beneficial for clearing airway obstructions in individuals with chronic respiratory conditions . 

Immune Modulation: Piper Longum has been shown to stimulate the immune response by activating macrophages and lymphocytes, which play a critical role in immune defense against infections

Nutraceuticals for Digestive Health: Due to its properties, it has been incorporated in the digestion enzyme blends with emphasis on the blends containing curcumin.

 Immune and Respiratory Supplements: Being an official expectorant and acting on the immune system, it is used in respiratory and immune affirmative preparations. 

Anti-inflammatory Supplements: Such as joint support and anti-inflammatory properties observed with Piper Longum Extract most supplements containing this extract are aimed at supporting joint health and inflammation .

6.Safety and Side Effects

Piper Longum Extract is relatively safe but side effects may present themselves when it is taken in large quantities; people should note that courses of any kind may have unwanted effects on the stomach. People on medication should seek advice from their doctors because the herb can interfere with drug metabolism owing to its enzyme inhibition properties.

Conclusion

The Piper Longum Extract is a mix of piperine, piperlongumine and the essential oil and has many medical benefits that’d been predicted by both cultural flexibility and research. Providing useful dietary and respiratory benefits and showing signs of possible anti- cancer properties, long pepper remains one of the most important ingredients in natural medicines today. Enduring positive effects with Piper Longum Extract on its therapeutic uses remain largely received in integrative medicine and other practices of wellness.

[cellbiologist]

FAM171A2 GRN NF κB Pathway TBBPA's Impa #researcher #sciencefather #bio...

[consultatiiladomiciliu-ro]

Cine spune ca albastrul de metilen face minuni in leziunile cerebrale - STUDII

Citeste articolul pe https://consultatiiladomiciliu.ro/cine-spune-ca-albastrul-de-metilen-face-minuni-in-leziunile-cerebrale-studii/

Cine spune ca albastrul de metilen face minuni in leziunile cerebrale - STUDII

Albastrul de metilen utilizat in mod curent ca antiseptic urinar (face urina verde sau albastra), are un rol salvator pentru creier. Citeste mai mult despre mecanismele prin care salveaza neuronii.

Neurological Mechanisms of Action and Benefits of Methylene Blue © Chase Hughes, Applied Behavior Research 2023 16

mitochondria after traumatic brain injury and are protected by cyclosporine A. Journal of neurotrauma, 34(7), 1291-1301. Lee, S. W., & Han, H. C. (2021).

Methylene blue application to lessen pain: its analgesic effect and mechanism. Frontiers in Neuroscience, 15, 663650. Liu, Y., Jin, W., Zhao, Y., Zhang, G., & Zhang, W. (2017).

Enhanced catalytic degradation of methylene blue by α-Fe2O3/graphene oxide via heterogeneous photo-Fenton reactions. Applied Catalysis B: Environmental, 206, 642-652. Matsuda, M., Huh, Y., & Ji, R. R. (2019).

Roles of inflammation, neurogenic inflammation, and neuroinflammation in pain. Journal of anesthesia, 33, 131-139. Miclescu, A. A., Svahn, M., & Gordh, T. E. (2015).

Evaluation of the protein biomarkers and the analgesic response to systemic methylene blue in patients with refractory neuropathic pain: a double-blind, controlled study. Journal of pain research, 387-397. Nakazawa, H., Chang, K., Shinozaki, S., Yasukawa, T., Ishimaru, K., Yasuhara, S., … & Kaneki, M. (2017).

iNOS as a driver of inflammation and apoptosis in mouse skeletal muscle after burn injury: possible involvement of Sirt1 S-nitrosylation-mediated acetylation of p65 NF-κB and p53. PloS one, 12(1), e0170391. Ola, M. S., Nawaz, M., & Ahsan, H. (2011).

Role of Bcl-2 family proteins and caspases in the regulation of apoptosis. Molecular and cellular biochemistry, 351, 41-58. Pan, H., Zhao, X., Lei, S., Cai, C., Xie, Y. Z., & Yang, X. (2019).

The immunomodulatory activity of polysaccharides from the medicinal mushroom Amauroderma rude (Agaricomycetes) is mediated via the iNOS and PLA2-AA pathways. International Journal of Medicinal Mushrooms, 21(8).

Neurological Mechanisms of Action and Benefits of Methylene Blue © Chase Hughes, Applied Behavior Research 2023 17 Rojas, J. C., Bruchey, A. K., & Gonzalez-Lima, F. (2012).

Neurometabolic mechanisms for memory enhancement and neuroprotection of methylene blue. Progress in neurobiology, 96(1), 32-45. Shen, J., Xin, W., Li, Q., Gao, Y., Yuan, L., & Zhang, J. (2019). Methylene blue reduces neuronal apoptosis and improves blood-brain barrier integrity after traumatic brain injury. Frontiers in Neurology, 10, 1133. Talley Watts, L., Long, J. A., Chemello, J., Van Koughnet, S., Fernandez, A., Huang, S., … & Duong, T. Q. (2014).

Methylene blue is neuroprotective against mild traumatic brain injury. Journal of neurotrauma, 31(11), 1063- 1071. Tucker, D., Lu, Y., & Zhang, Q. (2018).

From mitochondrial function to neuroprotection—an emerging role for methylene blue. Molecular neurobiology, 55, 5137-5153. Wang, W. X., Sullivan, P. G., & Springer, J. E. (2017).

Mitochondria and microRNA crosstalk in traumatic brain injury. Progress in Neuro- Psychopharmacology and Biological Psychiatry, 73, 104-108. Yadav, S., & Surolia, A. (2019).

Lysozyme elicits pain during nerve injury by neuronal Toll-like receptor 4 activation and has therapeutic potential in neuropathic pain. Science translational medicine, 11(504), eaav4176. Yonutas, H. M., Vekaria, H. J., & Sullivan, P. G. (2016).

Mitochondrial specific therapeutic targets following brain injury. Brain research, 1640, 77- 93. Zhang, D. X., Ma, D. Y., Yao, Z. Q., Fu, C. Y., Shi, Y. X., Wang, Q. L., & Tang, Q. Q. (2016).

ERK1/2/p53 and NF-κB dependent-PUMA activation involves in doxorubicin-induced cardiomyocyte apoptosis. Eur Rev Med Pharmacol Sci, 20(11), 2435-2442. Zhao, M., Liang, F., Xu, H., Yan, W., & Zhang, J. (2016).

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[colinwilson11]

Necrotising Enterocolitis Market Will Grow At Highest Pace Owing To Rising Prevalence Of Preterm Birth Complications

Necrotising enterocolitis (NEC) is a devastating gastrointestinal disease that primarily affects premature infants. It is characterized by inflammation and necrosis of the intestine. The risk factors associated with NEC include prematurity, formula feeding, and bacterial colonization of the intestine. Infants with very low birth weights have the highest risk. NEC treatment involves management of sepsis, support of vital organ function, bowel rest with no oral feeding, and surgery if necessary.

The Necrotising Enterocolitis Market is estimated to be valued at US$ 7.10 Bn in 2024 and is expected to exhibit a CAGR of 5.6% over the forecast period 2024-2031.

Key Takeaways

Key players operating in the Necrotising Enterocolitis market are AbbVie, AstraZeneca, Baxter International, Bristol-Myers Squibb, Fresenius Kabi. Rising prevalence of preterm birth complications globally is expected to drive the growth of the market during the forecast period. According to the World Health Organization, preterm birth complications are the leading cause of death among children under 5 years of age, responsible for approximately 1 million deaths in 2015. Technological advancements in parenteral nutrition and minimal invasive surgery have provided improved treatment outcomes for NEC.

Market Trends

Increasing research on nutraceuticals and probiotics for NEC prevention: Several clinical studies are evaluating the role of pre and probiotics such as Lactobacillus and Bifidobacterium in reducing the risk of NEC in preterm infants. This presents an opportunity for novel prevention strategies.

Rising adoption of minimal invasive surgery: Advancements in minimal invasive surgical techniques such as laparoscopy has resulted in reduced recovery time and complications for NEC patients undergoing surgery. This trend is expected to drive the future demand.

Market Opportunities

Development of novel therapeutics targeting inflammatory pathways: Researchers are investigating potential drug targets such as Toll-like receptor 4 (TLR4) and nuclear factor kappa B (NF-κB) signaling pathways to develop novel anti-inflammatory therapies for NEC treatment.

Increasing healthcare expenditure on pediatric care in emerging nations: Emerging countries in Asia Pacific and Latin America are witnessing increased healthcare spending focused on neonatal and pediatric care. This will propel the growth of therapeutics and medical devices market for pediatric gastrointestinal conditions.

Impact Of COVID-19 On Necrotising Enterocolitis Market Growth

The COVID-19 pandemic has adversely impacted the growth of the necrotising enterocolitis market globally. During the peak of pandemic in 2020-2021, the concentration of healthcare resources towards treatment of COVID-19 patients has negatively affected the diagnosis and treatment of other health conditions including necrotising enterocolitis. This led to reduction in number of surgeries and procedures carried out for necrotising enterocolitis management. Moreover, restrictions on non-essential healthcare services along with fear of virus spread stopped patients from visiting hospitals even for emergency cases. This impacted the market growth negatively during the period.

However, with gradual lift of restrictions in 2022 and availability of COVID-19 vaccines, the market is recovering slowly. The healthcare facilities are focusing on clearing backlog of non-COVID cases and regaining lost momentum in treatment of other diseases. The manufacturers are expanding supply chain capabilities and ramping up production to meet the increasing demand. Various initiatives are being taken by governments and healthcare organizations to raise awareness about timely management of necrotising enterocolitis. This will potentially boost the market in the coming years.

The United States holds the major share of necrotising enterocolitis market in terms of value, owing to large patient population, high treatment cost and adequate reimbursement framework. The region accounted for over 35% revenue share of global market in 2024.

Asia Pacific region is poised to witness fastest growth during the forecast period. Factors such as increasing healthcare expenditure, rising medical tourism, growing birth rate and expanding private hospital infrastructure will aid the market growth in Asia Pacific. China, India and Japan are emerging as profitable markets for necrotising enterocolitis treatment.

Get more insights on this topic: https://www.trendingwebwire.com/necrotising-enterocolitis-market-is-estimated-to-witness-high-growth-owing-to-advancements-in-parenteral-nutrition-solutions-and-devices/

About Author:

Ravina Pandya, Content Writer, has a strong foothold in the market research industry. She specializes in writing well-researched articles from different industries, including food and beverages, information and technology, healthcare, chemical and materials, etc. (https://www.linkedin.com/in/ravina-pandya-1a3984191)

What Are The Key Data Covered In This Necrotising Enterocolitis Market Report?

:- Market CAGR throughout the predicted period

:- Comprehensive information on the aspects that will drive the Necrotising Enterocolitis Market's growth between 2024 and 2031.

:- Accurate calculation of the size of the Necrotising Enterocolitis Market and its contribution to the market, with emphasis on the parent market

:- Realistic forecasts of future trends and changes in consumer behaviour

:- Necrotising Enterocolitis Market Industry Growth in North America, APAC, Europe, South America, the Middle East, and Africa

:- A complete examination of the market's competitive landscape, as well as extensive information on vendors

:- Detailed examination of the factors that will impede the expansion of Necrotising Enterocolitis Market vendors

FAQ’s

Q.1 What are the main factors influencing the Necrotising Enterocolitis Market?

Q.2 Which companies are the major sources in this industry?

Q.3 What are the market’s opportunities, risks, and general structure?

Q.4 Which of the top Necrotising Enterocolitis Market companies compare in terms of sales, revenue, and prices?

Q.5 Which businesses serve as the Necrotising Enterocolitis Market’s distributors, traders, and dealers?

Q.6 How are market types and applications and deals, revenue, and value explored?

Q.7 What does a business area’s assessment of agreements, income, and value implicate?

*Note: 1. Source: Coherent Market Insights, Public sources, Desk research 2. We have leveraged AI tools to mine information and compile it