#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

[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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［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

[didanawisgi]

SARS-CoV-2 Spike Targets USP33-IRF9 Axis via Exosomal miR-148a to Activate Human Microglia

SARS-CoV-2, the novel coronavirus infection has consistently shown an association with neurological anomalies in patients, in addition to its usual respiratory distress syndrome. Multi-organ dysfunctions including neurological sequelae during COVID-19 persist even after declining viral load. We propose that SARS-CoV-2 gene product, Spike, is able to modify the host exosomal cargo, which gets transported to distant uninfected tissues and organs and can initiate a catastrophic immune cascade within Central Nervous System (CNS). SARS-CoV-2 Spike transfected cells release a significant amount of exosomes loaded with microRNAs such as miR-148a and miR-590. microRNAs gets internalized by human microglia and suppress target gene expression of USP33 (Ubiquitin Specific peptidase 33) and downstream IRF9 levels. Cellular levels of USP33 regulate the turnover time of IRF9 via deubiquitylation. Our results also demonstrate that absorption of modified exosomes effectively regulate the major pro-inflammatory gene expression profile of TNFα, NF-κB and IFN-β. These results uncover a bystander pathway of SARS-CoV-2 mediated CNS damage through hyperactivation of human microglia. Our results also attempt to explain the extra-pulmonary dysfunctions observed in COVID-19 cases when active replication of virus is not supported. Since Spike gene and mRNAs have been extensively picked up for vaccine development; the knowledge of host immune response against spike gene and protein holds a great significance. Our study therefore provides novel and relevant insights regarding the impact of Spike gene on shuttling of host microRNAs via exosomes to trigger the neuroinflammation.

[nikshahxai]

Science & Medical Research | Hashnode Books | Nik Shah | Part 1

25. Mastering the Erector Spinae

Paragraph 1: The erector spinae group stabilizes and extends the spine, crucial for posture and lifting mechanics. This title highlights exercises and preventative measures for back health. Paragraph 2: Clinical perspectives delve into herniation, scoliosis management, and ergonomic solutions for chronic back pain. Read further at Mastering the Erector Spinae.

26. Mastering Penile Cancer: Harnessing Full Potential and Preventing Any Loss from Elongation

Paragraph 1: Penile cancer, though rare, can be life-altering. This work discusses early detection, medical interventions, and reconstructive techniques aimed at preserving function and self-esteem. Paragraph 2: Readers also learn about risk factors like HPV, emphasizing holistic prevention strategies that include vaccination and regular screenings. Gain knowledge at Mastering Penile Cancer.

27. Saksid Yingyongsuk: Mastering the Hemoglobin

Paragraph 1: Hemoglobin, the oxygen-carrying protein in red blood cells, is critical for sustaining life. This book describes its molecular structure and common disorders like sickle cell disease or thalassemia. Paragraph 2: By highlighting transfusion medicine and targeted therapies, it underscores ongoing research shaping future treatments. Explore more at Mastering the Hemoglobin.

28. Saksid Yingyongsuk: Mastering Plasma Replacement Therapy

Paragraph 1: Plasma replacement therapy, including plasma exchange, has transformative impacts on autoimmune conditions and organ failures. This guide dissects protocols, benefits, and potential complications. Paragraph 2: Real patient stories illustrate how timely interventions can drastically enhance recovery, bridging clinical expertise and compassionate care. Learn further at Mastering Plasma Replacement Therapy.

29. Dihydrotestosterone (DHT): Mastering Endocrinology

Paragraph 1: DHT is a potent androgen affecting hair growth, libido, and prostate health. This book clarifies how hormonal imbalances lead to conditions like androgenetic alopecia or benign prostatic hyperplasia. Paragraph 2: It highlights evidence-based treatments, from 5-alpha-reductase inhibitors to lifestyle adaptations, supporting balanced endocrine function. Delve deeper at DHT: Mastering Endocrinology.

30. Mastering Influenza: Understanding, Preventing, and Conquering the Common Cold

Paragraph 1: Influenza and the common cold affect millions yearly. This text distinguishes between viral strains, explaining how the flu can become severe or trigger global pandemics. Paragraph 2: Through vaccination insights and hygiene tips, it underscores prevention while detailing supportive care and antiviral options for active infections. Explore more at Mastering Influenza.

31. Mastering Mycobacteria and Meningitis

Paragraph 1: Mycobacteria—including tuberculosis—cause persistent infections, whereas meningitis inflames the membranes around the brain and spinal cord. This guide clarifies testing methods and advanced treatments. Paragraph 2: It emphasizes the significance of early intervention and global health strategies aimed at reducing transmission and mortality. Learn more at Mastering Mycobacteria and Meningitis.

32. Non-Lethal COVID King: Mastering the Coronavirus

Paragraph 1: Navigating the COVID-19 landscape involves understanding virus transmission, variants, and vaccine development. This resource offers a balanced view of how to prevent and mitigate the disease’s impact. Paragraph 2: It compares global responses, spotlighting success stories and highlighting collaborative research to curtail future outbreaks. Check out Non-Lethal COVID King.

33. Mastering NIK Deficiency: Autoimmune Disorders

Paragraph 1: NIK (NF-κB-inducing kinase) deficiency can trigger autoimmune abnormalities. This book dissects the molecular pathways behind immune system malfunctions and potential gene therapies. Paragraph 2: By analyzing clinical trials, it provides a forecast of how novel treatments may halt disease progression and alleviate symptoms. Discover more at Mastering NIK Deficiency.

34. Mastering Cancer, COVID-19, and Tuberculosis: Harnessing the Coronavirus, Tumors, and Disease Management

Paragraph 1: Drawing parallels between cancer, COVID-19, and TB, this guide highlights shared aspects of immune evasion and infection control. It explains synergy in global health strategies. Paragraph 2: Chapters offer advanced protocols for screening, immunotherapy, and containment measures, fostering an interconnected approach. Learn further at Mastering Cancer, COVID-19, and Tuberculosis.

35. Nik Shah: Mastering Radiotherapy and Chemotherapy

Paragraph 1: Radiotherapy and chemotherapy remain pillars of cancer treatment. This title examines their modes of action, side-effect profiles, and how combination therapies enhance efficacy. Paragraph 2: Personalized medicine approaches, including biomarker testing, are discussed for precision dosing and minimized toxicity. Gain knowledge at Mastering Radiotherapy and Chemotherapy.

36. Nik Shah: Mastering Red Blood Cells – The Science of Oxygen Transport and Cellular Health

Paragraph 1: Red blood cells ferry oxygen throughout the body, essential for vitality. This resource details their lifecycle, from erythropoiesis to senescence, linking disorders like anemia or polycythemia. Paragraph 2: It also spotlights dietary factors, supplementation, and emerging therapies that bolster RBC longevity and function. Find out more at Mastering Red Blood Cells.

37. Nik Shah: Understanding White Blood Cells – Unlocking the Key to Immunity

Paragraph 1: White blood cells, or leukocytes, defend against pathogens and manage inflammation. This text breaks down lymphocytes, neutrophils, and other subtypes crucial for overall immunity. Paragraph 2: Clinical examples illustrate how to track WBC counts, diagnose infections, and implement targeted immunotherapies. Dive deeper at Understanding White Blood Cells.

38. Nik Shah: Mastering Prostate Cancer & Prostatitis – Empowering Your Journey to Health and Healing

Paragraph 1: Prostate cancer and prostatitis pose significant challenges for men’s health. This title reviews early detection, biopsy protocols, and integrative treatment plans—including surgery and hormone therapy. Paragraph 2: Alongside conventional approaches, it highlights lifestyle modifications that bolster immune function and minimize recurrence. Learn at Mastering Prostate Cancer & Prostatitis.

39. Nik Shah: Mastering Brain Cancer – Strategies for Survival and Hope

Paragraph 1: Brain cancer demands unique strategies due to the blood-brain barrier and localized complexity. This book explores surgical advancements, radiotherapy precision, and targeted drug delivery. Paragraph 2: Patient stories illuminate resilience and highlight collaborative approaches between neurosurgeons, oncologists, and allied professionals. Find more at Mastering Brain Cancer.

40. Nik Shah: Mastering Stroke Recovery – Comprehensive Strategies for Full Recovery After Brain Hemorrhages

Paragraph 1: Stroke recovery hinges on timely intervention, rehabilitation intensity, and supportive care. This guide addresses hemorrhagic stroke specifics and outlines proven neuroplasticity techniques. Paragraph 2: From physical therapy regimens to cutting-edge robotic aids, it underscores a holistic journey back to daily independence. Read on at Mastering Stroke Recovery.

41. Nik Shah: Mastering Full Recovery from Traumatic Brain Injury (TBI)

Paragraph 1: Traumatic brain injury can disrupt cognition, mobility, and emotional health. This text emphasizes early diagnosis, progressive rehab, and family support as critical to full recovery. Paragraph 2: Integrating technology—like VR-based therapies and wearable sensors—enables more personalized and proactive healing. Investigate further at Mastering Full Recovery from TBI.

42. Gastronomy, Urology, Hematology, and Physiology: Exploring the Interconnections Between Diet, Health, and Body Functions

Paragraph 1: This cross-disciplinary resource links gastronomy (food science), urology (urinary system), hematology (blood health), and general physiology. By highlighting their synergy, it underscores balanced diets’ role in holistic well-being. Paragraph 2: Real-case examinations illustrate how nutrient intake influences kidney function, blood composition, and systemic vitality. Learn about these connections at Gastronomy, Urology, Hematology, and Physiology.

43. Mastering Brain Abscess & Pneumonia: A Comprehensive Guide to Diagnosis, Treatment, and Recovery

Paragraph 1: Brain abscesses and pneumonia, though distinct, share infectious roots that demand precise antimicrobial strategies. This guide explores advanced diagnostic imaging and lab tests. Paragraph 2: Treatment sections cover antibiotic regimens, surgical drainage where necessary, and rehabilitative steps to restore functionality. Discover more at Mastering Brain Abscess & Pneumonia.

44. Nik Shah: Mastering Neurodegenerative Diseases – A Comprehensive Guide to Understanding Diagnosis and Treatment

Paragraph 1: Neurodegenerative diseases, like Alzheimer’s and Parkinson’s, involve progressive neuron loss. This book unpacks genetic and environmental risk factors, plus early detection methods. Paragraph 2: Readers learn about symptom management, emerging therapies, and supportive care aimed at maintaining quality of life. Explore more at Mastering Neurodegenerative Diseases.

45. Mastering Inorganic Chemistry

Paragraph 1: Inorganic chemistry covers elements and compounds pivotal for medical imaging, drug synthesis, and industrial applications. This text simplifies atomic structures, bonding, and reaction mechanisms. Paragraph 2: Chapters highlight real-world scenarios—from metal-based catalysts to biominerals—bridging theory with practical usage. Delve into Mastering Inorganic Chemistry.

46. Mastering Common Elements: Hydrogen, Carbon, Nitrogen, Oxygen, and More

Paragraph 1: Hydrogen, carbon, nitrogen, and oxygen anchor life’s chemistry. This guide explores their roles in organic synthesis, atmospheric processes, and biological systems. Paragraph 2: Each element’s industrial and medical relevance is showcased, underscoring how fundamental building blocks shape daily life. Read more at Mastering Common Elements.

47. Mastering Darwinism & Evolution: A Guide to Patience, Resilience, and Serenity

Paragraph 1: Evolutionary principles stretch beyond biology, offering insights into adaptability in changing environments. This book ties Darwinism to modern concepts like resilience and mental serenity. Paragraph 2: By applying evolutionary logic to personal growth, readers refine strategies for problem-solving, forging robust mindsets. Learn how at Mastering Darwinism & Evolution.

48. Mastering Air Suspensions: Severing the Suspensory Ligament

Paragraph 1: Air suspensions, though typically linked to automotive systems, serve as an analogy for critical stabilizing structures. This text explores the concept of “severing the suspensory ligament” in medical contexts—addressing mobility, posture, or surgical procedures. Paragraph 2: It breaks down the biomechanics, examining how targeted interventions can alleviate tension or correct deformities without undermining integral support. Dive in at Mastering Air Suspensions.

[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/.

[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

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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).

Methylene blue exerts a neuroprotective effect against traumatic brain injury by promoting Neurological Mechanisms of Action and Benefits of Methylene Blue © Chase Hughes, Applied Behavior Research 2023 18 autophagy and inhibiting microglial activation. Molecular medicine reports, 13(1), 13-20. Zhu, Y., Wang, H., Fang, J., Dai, W., Zhou, J., Wang, X., & Zhou, M. (2018). SS-31 provides neuroprotection by reversing mitochondrial dysfunction after traumatic brain injury.

Oxidative Medicine and Cellular Longevity, 2018. Zhou, Y., Shao, A., Xu, W., Wu, H., & Deng, Y. (2019). Advance of stem cell treatment for traumatic brain injury. Frontiers in cellular neuroscience, 13, 301.

[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.

[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

[morriganpostofficial]

Unfold the 5 Unique Health Benefits of Lotus Leaf Tea

Lotus leaf tea, derived from the Nelumbo nucifera plant, is recognized for its myriad health benefits. Initially, it contains powerful antioxidants like flavonoids and carotenoids that protect against cellular aging and boost cardiovascular health. Next, its anti-inflammatory properties, mediated through the JNK/NF-κB pathway, support reduce systemic inflammation. Thirdly, tea regulates blood…

[rodneygoodie]

Osseointegration and Dental Implants

Dental implants can address missing teeth for individuals. An estimated three million Americans have dental implants, which grows annually. Osseointegration helps the implant adhere to the jawbone to remain in place after the procedure.

During the dental implant procedure, dental professionals place a screw-like fixture made of titanium in the jaw. This fixture acts as a replacement tooth root and enables the sturdy and permanent placement of a replacement tooth on the implant post. During treatment and implantation, dental professionals aim to ensure close contact with the jawbone, allowing for osseointegration. It ensures that the teeth implants become stable and anchored as the jawbone cells extend up to the implant and securely grip it. This process can take anywhere from six weeks to six months as the supportive root-like structure fully integrates with the jawbone.

The roots of osseointegration extend to 1952, when Professor Per-Ingvar Branemark, a Swedish orthopaedic surgeon, researched microcirculation. Branemark had inserted a titanium tube from an optical device into a rabbit's leg. When he attempted to remove the tube from the leg, Branemark discovered that the titanium and bone had fused, creating a “direct structural and functional connection between ordered living bone and the surface of a load-carrying implant.” After over a decade of research into osseointegration, which stems from the Greek osteon or bone, and the Latin word integrate or to make whole, Professor Branemark successfully performed the first titanium dental implant in 1965.

Once the area of the dental implant heals, the implants help reduce bone loss. They help individuals maintain a normal chewing function, which remains essential to a healthy, functional jawbone. Missing teeth can cause deterioration of underlying bone as chewing stimulation no longer occurs. Dentures do not have the same positive impact on the jawbone. They place pressure on the gums during chewing, which curtails blood supply, accelerating bone loss.

Cell signaling pathways define how the body reacts to implanted biomaterials through various responses. In a complex, non-linear series of reactions, the cells respond to extracellular signals by regulating intracellular gene expression. The biochemical responses or enzyme-catalyzed protein activations involve a cascading formation of activated proteins that engage in “cross-talk." The process relays information between the cells and transfers it from receptors to targets in the cell, such as mitochondria or nuclei.

A harmoniously coordinated activity, signaling pathways enable cellular responses that underpin human development, immunity, and tissue repair in adults. The osseointegration process captures two of these responses. In the early stages, the immune-inflammatory system modulates cellular responses, treating the implant as a foreign body within its microenvironment. A primary signaling pathway centers on the inflammatory Nuclear Factor Kappa B (NF-κB). Subsequent Wnt cell reactions regulate bone formation.

Titanium implants encourage biointegration by having immunomodulatory properties that respond to the immune-modulated inflammatory process. The biologically active presence of foreign body giant cells and macrophages makes the osseointegration process dynamic rather than static.

While healing, smoking negatively impacts the osseointegration process, impeding healing, bone cell growth, and blood flow and increasing the ultimate potential for implant failure. Lack of dental care and excessive alcohol consumption can also impact the long-term integrity of dental implants.

[y2fear]

Quercetin-loaded mesoporous nano-delivery system remodels osteoimmune microenvironment to regenerate alveolar bone in periodontitis via the miR-21a-5p/PDCD4/NF-κB pathway | Journal of Nanobiotechnology

[dhakshin-ayurveda]

Curcuma Longa Rhizome Powder: The Golden Spice with Remarkable Health Benefits

Introduction

Curcuma longa is an important plant of the ginger family that is commonly known as turmeric. When dried and ground into powder, the rhizome has been used as spice, dye and has medicinal value for many centuries. commonly referred to as the ‘Golden spice,’ turmeric contains several pharmacological agents, [curcuminoids], with curcumin being the most researched for its antioxidant effect, anti-inflammation, antimicrobial action, & anticancer properties, etc. This blog looks at the chemical constitution, therapeutic properties, and the source, which backs up the use of turmeric rhizome powder from the conventional and contemporary medication.

1.Historical and Traditional Uses

Ayurveda and Traditional Medicine

Haridra is the term used in Ayurvedic science for turmeric, and it is one of the most useful spices. It is taken to maintain the doshas; Vata, Pitta and Kapha and in managing conditions such as skin diseases, respiratory complaints and gastrointestinal complaints. Turmeric is also utilized in non Surgical formulations such as Haridra Khand in allergies, Kumudakshi taila for skin.

Cultural Significance

In India turmeric is associated with purity and wealth, and is used in religious rites, in weddings and other celebrations. It has also been used for wound and infection treatments traditionally, due to the presence of antiseptic characteristics in it.

2.Chemical Composition of Curcuma Longa Rhizome Powder

The therapeutic potential of turmeric lies in its diverse phytochemical composition, including:

Curcuminoids (2–5%) Curcumin (C₂₁H₂₀O₆): The primary bioactive compound responsible for turmeric’s bright yellow color and potent health benefits.

Demethoxycurcumin and bisdemethoxycurcumin: Curcuminoids with complementary effects to curcumin.

2. Volatile Oils (4–14%): Includes turmerone, zingiberene, and ar-turmerone, which contribute to its anti-inflammatory and antimicrobial properties .

Polysaccharides Known for their immunomodulatory and anti-ulcer effects.

Proteins and Resins Play a role in turmeric’s therapeutic effects on digestion and skin health.

3.Health Benefits of Curcuma Longa Rhizome Powder

a)Potent Anti-inflammatory Effects

Inflammation is a major cause of diseases including arthritis, diabetes and cardiovascular diseases and turmeric is used therapeutically to reduce chronic inflammation.

Mechanism of Action: Curcumin also suppresses the expression of enzymes involved in COX-2 and LOX and the NF-κB signaling pathway which is involved in TNF-α and IL-6 cytokines .

Evidence: Research indicates that administration of turmeric modestly decreases pain and inflammation in patients suffering from osteoarthritis similar to NSAIDs but less side effects.

b) It is an Efficient AntiOxidant Substrate chronic inflammation, a key contributor to diseases like arthritis, diabetes, and cardiovascular conditions

b)Powerful Antioxidant Properties

Curcumin is a strong antioxidant, protecting cells from oxidative stress caused by free radicals.

Mechanism: It neutralizes reactive oxygen species (ROS) and enhances the activity of endogenous antioxidant enzymes like superoxide dismutase (SOD) and catalase .

•Evidence: Research confirms that turmeric supplementation reduces markers of oxidative stress in conditions such as diabetes and metabolic syndrome .

c)Digestive Health and Liver Protection

Turmeric strengthens the intestinal lining and has antioxidants that neutralize toxic substances and reduce liver oxidative stress.

Bile Production: It aids in bile production and therefore prevents cases of bloating and indigestion in most people who take it.

Hepatoprotective Effects: Curcumin blocks the inflammation of hepatocytes and free radicals that causes liver damage. Research writes it down in ways such as in non-alcoholic fatty liver disease (NAFLD)

d)Cardiovascular Benefits

Recent studies also show that curcumin helps support cardiovascular health by maintaining lipid levels and decreasing inflammation.

•Cholesterol Regulation: To date, clinical studies highlight that turmeric decreases levels of LDL cholesterol and triglycerides and at the same time increases levels of HDL cholesterol.

•Blood Pressure Control: It’s an arterial dilator associated with nitric oxide that enhances the ability of arteries to dilate hence enhancing blood flow

e) Skin and Wound Healing

It has been used in the past in treating various skin disorders including wound, eczema and psoriasis.

Antimicrobial Action: It also has abilities of combating infections since the growth of bacteria, fungi and virus is prevented by curcumin.

SkinRegeneration: It has an anti-inflammatory effect and stimulates the production of collagen therefore enhancing speedy healing and little scarring .

f) Immune System Support

Turmeric increases the function of the immune cells by regulating its activity.

Immunomodulatory Effects: It increases the activity of macrophages T- cells, and Natural killer (NK)cells Fig. 1.

AntiviralProperties: Research also shows that curcumin can delay the viral replication in such virus infections as influenza and hepatitis.

g) Anti-cancer Potential

Curcumin is investigated for its potential to prevent as well as cure different types of cancer rampantly.

Induction of Apoptosis: It targets the cancer cells for apoptosis without affecting non cancerous cells .

Angiogenesis Inhibition: Tumour growth requires formation of new blood vessels, which this drug is able to inhibit, reducing cancer development .

4. Mechanisms of Action

Mechanisms of Action Enzyme Inhibition: It suppresses some synthesis of inflammatory mediators such as COX-2 and LOX which lower inflammation.

Gene Regulation: Regulates genes with inflammatory response, oxidation, and cell survival including knocking down NF-κB and MAPK.

Antioxidant Defense: Increases the body’s natural antioxidant level as well as neutralizing free radicals.

Cellular Protection: Antioxidant, shields DNA and cell membranes to reverse effect of chronic diseases

5. Modern Applications of Curcuma Longa Rhizome Powder

Nutraceuticals: It helps in mixtures used in supplements for treating joint aches, boosting immunity and general body health.

Functional Foods: Consumed as a wellness supplement in golden milk, teas, and energy bars.

Cosmetics: Used together with skincare products for it also has anti-inflammatory and skin illuminating properties.

Pharmaceuticals: Also incorporated in preparations for control of inflammatory and metabolic diseases

6.Safety and Recommended Dosage

Safety Profile

However, the common yellow spice, turmeric, is safe for consumption. There are always side effects of most supplements especially when taken in large quantities and this may include a rise in heart rate and mild gastric upsets.

Recommended Dosage

For general wellness: 500–2,000 mg of curcumin daily, standardized to 95% curcuminoids.

Always consult a healthcare provider before starting supplementation, especially if on medication or pregnant.

Conclusion

Curcuma longa rhizome powder is the golden spice of India containing curcuminoids and a variety of bioactive compounds that are recommended in traditional medicine practice and supported by scientific evidence. With its cleansing and anti-inflammatory and antioxidant effects, digestive health benefits through demonstration of boost to immunity as well as chronic disease relief, turmeric still holds its status as a natural remedy. From cooking to beverages and supplements to skincare products, turmeric is still pushing its curcumin cure for a healthier you.