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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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fivehundredwords · 2 years ago

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Alzheimer's Disease: biomarkers and neuroimaging markers cheatsheet for research articles

As Alzheimer's Disease (AD) research skews toward understanding the brain than the pathogenic proteins, studies exploring biomarkers and neuroimaging are hopeful toward developing a method for successful prevention of AD. A biomarker is a molecule, whose presence indicates abnormality or disease, and thus, is crucial in diagnostic procedures. Levels of certain molecules is notably altered in cerebrospinal fluid and in blood plasma, which helps in diagnosing the occurrence of AD. Neuroimaging involves the use of techniques such as magnetic resonance imaging and computed tomography to observe neuronal activity in the brain. This is good news, especially for AD, as the asymptomatic stage of the disease can be identified early enough.

Although the exact function and involvement in clinical practice is not profuse, altered concentrations of these biomarkers in plasma or cerebrospinal fluid encourage further research:

Amyloid and tau serve as the unsurprising biomarkers of AD pathology.

Neurofilament-light chain (NF-L) and visinin-like protein-1 (VILIP-1) are the most promising biomarkers of neuronal injury.

Post-synaptic protein neurogranin (Ng) and pre-synaptic proteins synaptosome-associated protein-25 (SNAP-25) and synaptotagmin-1 (Syt-1) are considered major biomarkers of synaptic injury.

Brain and CSF levels of tumor necrosis factor alpha (TNF-α) and increased levels of interleukin group of proteins (ILs) indicate intensified microglial response to neuroinflammation.

TREM2 receptor and YKL-40 glycoprotein are also reliable indicators of inflammation and impaired clearance of amyloid beta.

Heart-type fatty acid-binding protein (hFABP) could be a marker for pathology in blood vessels supplying the brain. Some vascular markers also show potential as markers of vascular injury in AD: von Willebrand factor (vWF) and monokine induced by γ-interferon (MIG, also known as CXCL-9).

Concentrations of TAR-DNA binding protein (TDP-43) in the brain and plasma and serum indicate, even contribute to, inflammation, mitochondrial dysfunction, and neuronal/synaptic injury in AD.

Neuroimaging techniques reveal structural, functional, and diffusion-related activities of the neurons. To identify them, markers are tracked in images obtained. Each marker is determined with the activity and biochemistry of the group of/individual neurons being studied.

Structural MRI will show location and severity of atrophy which can be identified in grey scale images by applying programs that create analogous color grading.

Functional MRI relies on blood oxygenation level dependent (BOLD) signal which reflects changes in blood oxygenation levels in response to neural activity.

Diffusion weighted imaging (DWI) focuses on diffusion of water molecules. A tensor model is applied to images obtained from DWI. The diffusion tensor imaging (DTI) metrics thus obtained help in studying connectivity through structural integrity of white matter tracts.

Tractography involves 3-D reconstruction of white matter as observed in DWI, which provides a more detailed look into a patient’s neural networks.

In positron emission tomography (PET), markers are identified and labelled so their features or functions can be traced during this procedure to obtain a resulting PET scan. The imaging procedure is named according to its marker: amyloid-PET, tau-PET, FDG-PET, inflammation-PET, receptor-PET.

FDA approved drugs Galantamine, Rivastigmine, and Donepezil alleviate symptoms such as memory loss and confusion in mild to moderate AD, although their effects seem to be negligible. They also cause nausea and vomiting as side effects and are not suitable for every patient. Recently approved drugs, Aducanumab and Lecanemab focus on removing accumulated amyloid. Their effectiveness is still doubted on the basis of studies finding that targeting amyloid has little to do with curbing the actual progression of the disease.

bibliography -

Tarawneh R. Biomarkers: our path towards a cure for Alzheimer disease. Biomarker insights. 2020 Nov;15:1177271920976367.

Cavedo E, Lista S, Khachaturian Z, Aisen P, Amouyel P, Herholz K, Jack Jr CR, Sperling R, Cummings J, Blennow K, O’Bryant S. The road ahead to cure Alzheimer’s disease: development of biological markers and neuroimaging methods for prevention trials across all stages and target populations. The journal of prevention of Alzheimer's disease. 2014 Dec;1(3):181.

Medications for Alzheimer's Disease Stanford Healthcare. Accessed 21-04-2023.

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eshas90 · 1 month ago

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blueoaknx · 1 month ago

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Mitochondria and Post-Traumatic Stress

The Connection Between Mitochondria and Post-Traumatic Stress Disorder (PTSD)

Introduction

Post-Traumatic Stress Disorder (PTSD) is a complex psychiatric condition that can manifest following exposure to traumatic events. While the psychological and behavioral dimensions of PTSD have been extensively explored, emerging evidence suggests a significant role of mitochondrial dysfunction in its pathophysiology. This article aims to provide a formal analysis of the relationship between mitochondria and PTSD, emphasizing mitochondrial mechanisms, neuroinflammatory processes, and potential therapeutic interventions.

Mitochondrial Function and Structure

Mitochondria are double-membraned organelles essential for cellular energy production, primarily through oxidative phosphorylation (OXPHOS). They contain their own circular DNA (mtDNA) and are responsible for synthesizing adenosine triphosphate (ATP) via the electron transport chain (ETC). Key functions of mitochondria include:

ATP Synthesis: Mitochondria generate ATP through a series of redox reactions facilitated by the ETC, which comprises complexes I-IV and ATP synthase.

Regulation of Metabolism: These organelles play a pivotal role in various metabolic pathways, including the tricarboxylic acid (TCA) cycle, fatty acid oxidation, and amino acid metabolism.

Apoptosis Regulation: Mitochondria release pro-apoptotic factors, such as cytochrome c, which are integral to the intrinsic pathway of apoptosis in response to cellular stress.

Calcium Homeostasis: Mitochondria modulate intracellular calcium levels, which are crucial for cellular signaling and neurotransmitter release.

Mitochondrial Dysfunction in Chronic Stress and PTSD

Chronic stress, a precursor to PTSD, has been shown to induce mitochondrial dysfunction through various mechanisms:

Impaired ATP Production: Chronic stress can result in mitochondrial bioenergetic failure, characterized by reduced ATP synthesis due to inhibited OXPHOS. This energy deficit adversely affects neuronal function and synaptic plasticity, contributing to cognitive and emotional dysregulation.

Increased Oxidative Stress: Stress-induced overproduction of reactive oxygen species (ROS) can overwhelm the cellular antioxidant defenses, leading to oxidative damage of mtDNA, proteins, and lipids. This oxidative stress has been implicated in the development of various psychiatric disorders, including PTSD.

Altered Mitochondrial Dynamics: Mitochondria undergo continuous fission and fusion, processes that are essential for maintaining mitochondrial function and integrity. Chronic stress can disrupt these dynamics, resulting in fragmented mitochondria and impaired function. Observations of altered mitochondrial morphology in PTSD may suggest a role in the disorder's pathology.

Dysregulation of Calcium Signaling: Mitochondrial calcium uptake is critical for regulating neurotransmitter release and neuronal excitability. Dysregulated calcium homeostasis due to mitochondrial dysfunction may contribute to the heightened anxiety and mood disturbances characteristic of PTSD.

Neuroinflammation and Mitochondrial Dysfunction

Neuroinflammation is a prominent feature of PTSD, characterized by the activation of microglia and the release of pro-inflammatory cytokines. Mitochondrial dysfunction has been implicated in amplifying neuroinflammatory responses:

Mitochondria as Regulators of Inflammation: Mitochondria play a crucial role in the activation of the NLRP3 inflammasome, a multiprotein complex that promotes the secretion of interleukin-1β (IL-1β) and IL-18. Dysfunctional mitochondria may increase ROS production, further activating microglia and exacerbating neuroinflammation.

Cytokine Release: Pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), can impair mitochondrial function, creating a feedback loop that sustains neuroinflammation and contributes to the persistence of PTSD symptoms.

Impact on Neural Circuitry: Neuroinflammation can disrupt neural circuitry, particularly in regions such as the amygdala and prefrontal cortex, which are critical for emotional regulation and fear processing. Such disruptions may lead to the hyperarousal and emotional dysregulation observed in PTSD.

Genetic and Epigenetic Influences

Genetic predisposition and epigenetic modifications can significantly influence mitochondrial function and the susceptibility to PTSD. Specific polymorphisms in genes associated with mitochondrial dynamics (e.g., PGC-1α, a key regulator of mitochondrial biogenesis) may affect an individual’s response to stress and trauma.

Epigenetic mechanisms, including DNA methylation and histone modifications, can be altered by environmental stressors, impacting mitochondrial gene expression. These changes may influence mitochondrial function, energy metabolism, and oxidative stress responses, thereby contributing to the pathophysiology of PTSD.

Therapeutic Implications

Understanding the relationship between mitochondrial dysfunction and PTSD offers several avenues for therapeutic intervention:

Mitochondrial-Targeted Antioxidants: Compounds such as MitoQ and SkQ1 are designed to selectively target mitochondria and mitigate oxidative stress. These agents may protect against mitochondrial damage and restore cellular function, potentially alleviating PTSD symptoms.

Exercise and Physical Activity: Regular physical activity enhances mitochondrial biogenesis and improves overall mitochondrial function. Exercise has been demonstrated to reduce oxidative stress and inflammation while promoting neurogenesis and synaptic plasticity, thus offering a comprehensive approach to mitigating PTSD.

Nutritional Interventions: Diets rich in antioxidants (e.g., vitamins C and E, polyphenols) and omega-3 fatty acids may support mitochondrial health and reduce neuroinflammation. Nutritional strategies can also improve mood and cognitive function, providing additional benefits for individuals with PTSD.

Pharmacological Approaches: Investigational drugs targeting mitochondrial function or enhancing energy metabolism hold promise for treating PTSD. Ongoing research into compounds that improve mitochondrial dynamics or protect against oxidative damage is critical.

Mindfulness and Stress Reduction Techniques: Interventions such as mindfulness meditation and cognitive behavioral therapy (CBT) may help mitigate chronic stress, potentially leading to improvements in mitochondrial function and overall mental health.

Conclusion

The intricate relationship between mitochondria and PTSD highlights the necessity for a comprehensive approach to understanding and treating this multifaceted disorder. Mitochondrial dysfunction appears to play a critical role in the physiological changes associated with PTSD, influencing energy metabolism, oxidative stress, and neuroinflammatory processes. By prioritizing mitochondrial health through lifestyle modifications, targeted therapies, and nutritional interventions, it may be possible to improve outcomes for individuals suffering from PTSD. Continued research is imperative to further elucidate these connections and explore novel therapeutic strategies aimed at addressing the underlying biological mechanisms of PTSD, ultimately paving the way for more effective treatments for this challenging condition.

#Mitochondria #Post-Traumatic Stress Disorder (PTSD)#Mitochondrial dysfunction #Oxidative phosphorylation (OXPHOS)#nutraceuticals

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moleculardepot · 3 months ago

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Recombinant Canine TNF-alpha

Recombinant Canine TNF-alpha Catalog number: B2017868 Lot number: Batch Dependent Expiration Date: Batch dependent Amount: 1 μg Molecular Weight or Concentration: ~17.3 kDa Supplied as: Powder Applications: a molecular tool for various biochemical applications Storage: -20°C Keywords: TNFA, cTNF, cachectin, tumor necrosis factor ligand superfamily member 2 Grade: Biotechnology grade. All products…

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medicapharmabv · 3 months ago

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The Role of Imiquimod in Dermatological Therapy: Benefits and Risks

Imiquimod is a versatile medication widely used in dermatology. This blog explores its benefits, potential risks, and why MedicaPharma is the preferred source for purchasing imiquimod.

Mechanism of Action

How Imiquimod Works:

Immune System Stimulation: Imiquimod activates toll-like receptors (TLRs) on immune cells. This activation triggers a cascade of immune responses, including the production of cytokines.

Cytokine Production: Key cytokines such as interferon-alpha, tumor necrosis factor-alpha (TNF-alpha), and interleukins are produced. These cytokines enhance the body’s ability to target and eliminate abnormal skin cells.

Targeting Abnormal Cells: The immune activation helps in clearing various skin conditions by promoting the destruction of infected or precancerous cells.

Benefits and Advantages

Key Benefits of Imiquimod:

Non-Invasive Treatment: Imiquimod is applied topically, offering a non-invasive alternative to surgical or other more invasive dermatological treatments.

Versatility: It is effective for a range of dermatological conditions, including viral infections like genital warts, precancerous lesions such as actinic keratosis, and certain skin cancers.

Convenient Application: The topical application of imiquimod is user-friendly and well-tolerated, making it a convenient option for patients.

Side Effects and Risks

Managing Side Effects:

Local Reactions: Common side effects include skin irritation, redness, and itching at the site of application. These are generally mild and manageable.

Systemic Symptoms: Although less common, systemic effects such as flu-like symptoms (fever, fatigue) can occur. Monitoring and consultation with a healthcare provider can help manage these risks.

Regular Monitoring: It is important to monitor for any adverse effects to ensure the treatment remains effective and comfortable for the patient.

Why Buy Imiquimod from MedicaPharma

The MedicaPharma Advantage:

Quality Assurance: MedicaPharma’s imiquimod is produced according to stringent GMP standards, ensuring high quality and efficacy.

Reliable Distribution: MedicaPharma offers consistent and reliable distribution, making it a trusted source for purchasing imiquimod.

Trusted Supplier: MedicaPharma’s commitment to quality and customer service positions them as a preferred choice for healthcare providers and patients.

Conclusion

Imiquimod is a valuable tool in dermatological therapy, offering a non-invasive and effective treatment for various skin conditions. For high-quality imiquimod, MedicaPharma is a dependable supplier that ensures optimal therapeutic outcomes.

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mitalipingale · 6 months ago

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The Tumor Necrosis Factor (TNF) Alpha Inhibitors Market in 2023 is US$ 41.88 billion, and is expected to reach US$ 44.35 billion by 2031 at a CAGR of 0.7%.

#Tumor Necrosis Factor (TNF) Alpha Inhibitors Market #Tumor Necrosis Factor (TNF) Alpha Inhibitors Market Forecast #Tumor Necrosis Factor (TNF) Alpha Inhibitors Market Overview

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suhaana240 · 3 months ago

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How to Activate Your Brain in the Morning for Maximum Productivity

Mornings can be a struggle, but learning how to activate your brain in the morning can set the tone for a productive day. Many people wonder if their brain works better in the morning, and the answer is often yes - with the right strategies. Just as athletes warm up before a game, individuals can benefit from morning brain exercises to fully wake up and kickstart their cognitive functions.

Jim Kwik, a renowned brain coach, emphasizes the importance of a morning routine to optimize brain performance. His approach combines physical activity, sensory stimulation, and nourishment to help people shake off grogginess and boost mental clarity. By incorporating these techniques, anyone can learn how to warm up their brain in the morning, leading to improved focus, creativity, and overall productivity throughout the day.

Establish a Consistent Morning Routine

Establishing a consistent morning routine is crucial for activating the brain and setting the tone for a productive day. Waking up at the same time every day, including weekends, helps improve sleep quality and reinforces the body's circadian rhythm 1. This consistency acts as a cue to the body about when to be awake and when to sleep 1.

To break the habit of hitting the snooze button, which can negatively affect physical health and increase stress 2, try these strategies:

Use a traditional alarm clock placed away from the bed 2

Count down 3-2-1 and sit up immediately 2

Expose yourself to natural light upon waking 2

Consistency in wake-up times can help stabilize learning, memory, and concentration capabilities 3. Ideally, aim to wake up by 7:00 AM and be ready for sleep by 10:00 PM 3. This routine allows the brain to transition through theta and alpha waves, priming it for peak performance 4.

Engage in Physical Activity

Physical activity in the morning has a significant impact on brain activation and overall productivity. Regular morning walks can boost immune function, improve circulation, and support joint health 5. Studies have shown that individuals who walk at least 20 minutes a day, five days a week, experience 43% fewer sick days 5. Moreover, walking two miles daily can reduce the risk of stroke 5.

High-intensity interval training (HIIT) has been linked to better memory and brain volume in older adults. A study found that HIIT workouts improved memory and preserved brain volume, with benefits lasting up to five years 6. HIIT sessions typically involve four-minute bouts of hard exercise at 80-95% of maximum heart rate, interspersed with three-minute recovery periods 6.

HIIT workouts can also reduce levels of tumor necrosis factor alpha (TNF-α), a protein associated with chronic inflammation, and increase levels of brain-derived neurotrophic factor (BDNF), which stimulates neuron growth and repair 6.

Stimulate Your Senses

Activating the senses in the morning can jumpstart the brain for maximum productivity. Light exposure plays a crucial role in regulating the body's circadian rhythm. Bright, blue-rich light in the morning promotes wakefulness and improves cognitive performance 7. To harness these benefits, individuals can spend time outdoors, sit near windows, or use light boxes 7.

Auditory stimulation through binaural beats can enhance focus and creativity. Listening to specific frequencies has been linked to reduced anxiety and improved concentration 8. For instance, binaural beats in the lower beta range (14 to 30 Hz) have been associated with increased alertness and problem-solving abilities

Aromatherapy can also boost productivity. Scents like lemon, peppermint, and eucalyptus have been found to promote concentration and mental clarity 9. In fact, a study showed that lemon fragrance in workspaces led to a 54% decrease in typing errors 10.

Nourish Your Body and Mind

Proper nutrition plays a crucial role in activating the brain for maximum productivity. A brain-boosting smoothie can provide essential nutrients to support cognitive function and mental clarity. This delicious concoction includes ingredients known to enhance focus, memory, and overall brain health 11.

Key components of a brain-boosting smoothie include:

Berries: Rich in antioxidants, particularly anthocyanins, which may improve cognitive function 11.

Banana: Provides natural sugars for quick energy and essential vitamins for brain health 11.

Avocado: Contains healthy fats that support blood flow and cognitive function 11.

Leafy greens: Packed with neuroprotective vitamins and minerals 11.

Turmeric: Contains curcumin, which has anti-inflammatory and antioxidant benefits 11.

These ingredients work together to provide a nutrient-dense start to the day, supporting brain health and overall well-being.

Conclusion

Activating your brain in the morning has a significant impact on your productivity throughout the day. By establishing a consistent routine, engaging in physical activity, stimulating your senses, and nourishing your body and mind, you can set yourself up for success. These strategies work together to shake off grogginess, boost mental clarity, and enhance focus.

Implementing these techniques is not just about improving your workday; it's about enhancing your overall well-being. The benefits extend beyond increased productivity to include better physical health, improved cognitive function, and reduced stress levels. By making these practices a part of your daily routine, you're investing in your long-term health and success, setting the stage to tackle challenges with a clear and energized mind.

Become “one” with the Universe in 7 mins

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precisionantibody · 4 months ago

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Advancing Healthcare: The Impact and Importance of Monoclonal Antibody Services

The Foundation of Monoclonal Antibodies

Monoclonal antibodies are laboratory-produced molecules engineered to serve as substitute antibodies that can restore, enhance, or mimic the immune system's attack on unwanted cells. Unlike polyclonal antibodies, which are derived from multiple cell lines and recognize multiple epitopes, monoclonal antibodies are produced from a single clone of cells and recognize a single epitope. This specificity allows for precise targeting of pathogens or diseased cells, minimizing damage to healthy tissues.

The production of monoclonal antibodies involves the fusion of an antibody-producing B-cell with a myeloma (cancer) cell, creating a hybridoma. This hybridoma can be cultured to produce large quantities of identical antibodies, which can then be purified and used in various therapeutic applications.

Applications in Medicine

One of the most notable applications of monoclonal antibody services is in oncology. Cancer treatments have been transformed by the introduction of monoclonal antibodies that can specifically target cancer cells. For instance, trastuzumab (Herceptin) is a monoclonal antibody used to treat HER2-positive breast cancer by binding to the HER2 receptor on cancer cells, inhibiting their growth and proliferation. Similarly, rituximab (Rituxan) targets the CD20 antigen on B-cells, making it effective in treating certain types of non-Hodgkin lymphoma and chronic lymphocytic leukemia.

Monoclonal antibodies have also made significant strides in the treatment of autoimmune diseases. Drugs like adalimumab (Humira) and infliximab (Remicade) target tumor necrosis factor-alpha (TNF-α), a cytokine involved in systemic inflammation. By inhibiting TNF-α, these monoclonal antibodies help manage conditions like rheumatoid arthritis, Crohn's disease, and psoriasis.

In infectious diseases, monoclonal antibodies have been used to provide passive immunity. For example, palivizumab (Synagis) is used to prevent respiratory syncytial virus (RSV) infections in high-risk infants. During the COVID-19 pandemic, monoclonal antibody therapies like bamlanivimab and casirivimab/imdevimab were developed to neutralize the SARS-CoV-2 virus, reducing the severity of symptoms and hospitalizations in infected patients.

The Development Process

Developing monoclonal antibodies involves several critical steps, starting with the identification of a suitable antigen. Once the target antigen is identified, researchers generate hybridomas that produce the desired antibody. These hybridomas are screened for specificity and affinity, and the best candidates are selected for further development.

The selected monoclonal antibodies undergo rigorous testing in preclinical models to assess their safety, efficacy, and pharmacokinetics. Successful candidates then move on to clinical trials, Anti Idiotype Monoclonal Antibody where they are tested in humans to determine their therapeutic potential. The entire process requires significant investment, expertise, and collaboration between academia, industry, and regulatory agencies.

Future Prospects

The future of monoclonal antibody services is promising, with ongoing research aimed at improving their efficacy, reducing side effects, and expanding their applications. Advances in genetic engineering and biotechnology are enabling the development of bispecific antibodies, antibody-drug conjugates, and other innovative formats that offer enhanced therapeutic benefits.

Moreover, personalized medicine is set to benefit from monoclonal antibodies, as they can be tailored to target specific biomarkers in individual patients. This approach promises to deliver more effective treatments with fewer side effects, ushering in a new era of precision healthcare.

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knowmybio123 · 6 months ago

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The Blood Tells All: Decoding Your Body's Inflammatory Signals

Inflammation is a crucial biological response to harmful stimuli, such as pathogens, damaged cells, or toxic compounds. While acute inflammation is a protective response, chronic inflammation can lead to various health problems, including cardiovascular disease, diabetes, and autoimmune disorders. Inflammatory blood markers are essential tools for diagnosing and monitoring these conditions. In this article, we will delve into the most significant inflammatory blood markers, their roles, and what they can tell us about our health.

What are Inflammatory Blood Markers?

Inflammatory blood markers are substances in the blood that indicate the presence of inflammation in the body. These markers can be proteins, cells, or other molecules that are produced in response to inflammation. Measuring these markers can help healthcare providers diagnose and monitor inflammatory conditions and diseases.

The Importance of Inflammatory Blood Markers

Understanding and monitoring inflammatory blood markers is vital for several reasons:

Early Detection: They can help detect inflammation before symptoms become severe.

Disease Monitoring: They are useful for tracking the progression of inflammatory diseases.

Treatment Efficacy: They can indicate how well a treatment is working.

Common Inflammatory Blood Markers

1. C-Reactive Protein (CRP)

C-Reactive Protein (CRP) is one of the most widely used inflammatory markers. It is produced by the liver in response to inflammation. Elevated levels of CRP can indicate acute inflammation and are associated with conditions like infections, autoimmune diseases, and chronic diseases such as cardiovascular disease.

2. Erythrocyte Sedimentation Rate (ESR)

The Erythrocyte Sedimentation Rate (ESR) measures how quickly red blood cells settle at the bottom of a test tube. A faster-than-normal rate may indicate inflammation. ESR is commonly used to monitor diseases like rheumatoid arthritis and lupus.

3. Interleukin-6 (IL-6)

Interleukin-6 (IL-6) is a cytokine that plays a crucial role in the immune response. Elevated levels of IL-6 are often found in patients with chronic inflammatory conditions, including autoimmune diseases and certain cancers.

4. Tumor Necrosis Factor-alpha (TNF-alpha)

Tumor Necrosis Factor-alpha (TNF-alpha) is another cytokine involved in systemic inflammation. High levels of TNF-alpha are linked to chronic inflammatory diseases such as Crohn's disease, psoriasis, and rheumatoid arthritis.

5. Fibrinogen

Fibrinogen is a blood plasma protein that's part of the coagulation process. Increased fibrinogen levels can indicate inflammation and are associated with a higher risk of cardiovascular diseases.

6. Ferritin

Ferritin is a blood protein that contains iron. Elevated ferritin levels can indicate inflammation, as it is an acute-phase reactant that increases in response to infection and inflammation.

7. Homocysteine

Homocysteine is an amino acid in the blood. Elevated levels of homocysteine are associated with inflammation and an increased risk of cardiovascular diseases.

8. Serum Amyloid A (SAA)

Serum Amyloid A (SAA) is a protein that increases in response to inflammation. High levels of SAA are found in patients with chronic inflammatory conditions and can be used to monitor disease activity.

9. White Blood Cell Count (WBC)

The White Blood Cell Count (WBC) measures the number of white blood cells in the blood. Elevated WBC counts can indicate infection or inflammation and are used to diagnose and monitor various conditions.

10. Procalcitonin

Procalcitonin is a peptide that increases significantly during bacterial infections and inflammation. It is a useful marker for diagnosing bacterial infections and sepsis.

How Inflammatory Blood Markers are Measured

Inflammatory blood markers are typically measured through blood tests. These tests can be performed in a laboratory or a healthcare provider's office. The process involves drawing a blood sample from a vein, usually in the arm, and analyzing it for specific markers.

Interpreting Inflammatory Blood Marker Results

The interpretation of inflammatory blood marker results depends on several factors, including the specific marker being measured, the patient's medical history, and the presence of other symptoms. Here are some general guidelines for interpreting these results:

CRP: Levels above 10 mg/L may indicate significant inflammation, while levels above 100 mg/L are often seen in severe infections or chronic inflammatory diseases.

ESR: Normal ranges vary by age and sex, but generally, an ESR above 20-30 mm/hr in adults may indicate inflammation.

IL-6: Elevated levels are typically seen in chronic inflammatory diseases and certain cancers.

TNF-alpha: High levels can indicate chronic inflammatory diseases.

Fibrinogen: Levels above 400 mg/dL may indicate inflammation.

Ferritin: Levels above 300 ng/mL in men and 200 ng/mL in women can indicate inflammation.

Homocysteine: Levels above 15 µmol/L are considered elevated.

SAA: Elevated levels are seen in chronic inflammatory conditions.

WBC: Counts above 11,000 cells/µL can indicate infection or inflammation.

Procalcitonin: Levels above 0.5 ng/mL can indicate bacterial infections or sepsis.

Conditions Associated with Elevated Inflammatory Blood Markers

Cardiovascular Diseases

Chronic inflammation is a key factor in the development of cardiovascular diseases. Elevated levels of CRP, fibrinogen, and homocysteine are commonly associated with an increased risk of heart attacks and strokes.

Autoimmune Diseases

Autoimmune diseases such as rheumatoid arthritis, lupus, and multiple sclerosis often result in elevated levels of inflammatory markers like CRP, ESR, and various cytokines.

Infections

Acute infections, both bacterial and viral, can cause significant increases in inflammatory markers. For example, elevated procalcitonin levels are often seen in bacterial infections and sepsis.

Cancer

Certain cancers can lead to elevated levels of inflammatory markers. IL-6 and TNF-alpha, in particular, are often elevated in various types of cancer.

Chronic Diseases

Chronic inflammatory diseases, including diabetes and chronic obstructive pulmonary disease (COPD), are associated with elevated levels of CRP, IL-6, and other markers.

Lifestyle Factors Affecting Inflammatory Blood Markers

Diet

A diet rich in fruits, vegetables, whole grains, and healthy fats can help reduce inflammation. Conversely, a diet high in processed foods, sugar, and unhealthy fats can increase inflammation.

Exercise

Regular exercise has been shown to reduce inflammation. Engaging in moderate physical activity for at least 30 minutes a day can help lower levels of inflammatory markers.

Stress

Chronic stress can lead to elevated levels of inflammatory markers. Practicing stress-reduction techniques such as meditation, yoga, and deep breathing can help manage inflammation.

Smoking and Alcohol

Smoking and excessive alcohol consumption are associated with increased inflammation. Quitting smoking and moderating alcohol intake can help reduce inflammation.

Treatments Targeting Inflammatory Blood Markers

Medications

Several medications are designed to reduce inflammation and lower inflammatory markers. These include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and specific biologic agents targeting cytokines like TNF-alpha and IL-6.

Lifestyle Changes

Lifestyle changes such as improving diet, increasing physical activity, and managing stress are effective ways to reduce inflammation and lower inflammatory markers.

Supplements

Certain supplements like omega-3 fatty acids, turmeric, and antioxidants can help reduce inflammation. However, it's essential to consult a healthcare provider before starting any supplement regimen.

Conclusion

Inflammatory blood markers are invaluable tools for diagnosing, monitoring, and managing various health conditions. By understanding these markers and their significance, we can take proactive steps to manage inflammation and improve our overall health. Regular check-ups, a healthy lifestyle, and proper medical care are essential components of managing inflammation and maintaining well-being.

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