cytochrome-c-t and Hepatitis

Non-alcoholic fatty liver disease (NAFLD) refers to any fatty liver disease that is not due to excessive use of alcohol. NAFLD probably results from abnormal hepatic lipid metabolism and insulin resistance. Aerobic exercise is shown to improve NAFLD. This review aimed to evaluate the molecular mechanisms involved in the beneficial effects of aerobic exercise on NAFLD.. We searched articles in English on the role of aerobic exercise in NAFLD therapy in PubMed.. The mechanisms of chronic aerobic exercise in regulating the outcome of NAFLD include: (i) reducing intrahepatic fat content by down-regulating sterol regulatory element-binding protein-1c and up-regulating peroxisome proliferator-activated receptor gamma expression levels; (ii) decreasing hepatic oxidative stress through modulating the reactive oxygen species, and enhancing antioxidant enzymes such as catalase and glutathione peroxidase; (iii) ameliorating hepatic inflammation via the inhibition of pro-inflammatory mediators such as tumor necrosis factor-alpha and interleukin-1 beta; (iv) attenuating mitochondrial dependent apoptosis by reducing cytochrome C released from the mitochondria to the cytosol; and (v) inducing hepato-protective autophagy.. Aerobic exercise, via different mechanisms, significantly decreases the fat content of the liver and improves the outcomes of patients with NAFLD.

Topics: Apoptosis; Autophagy; Cytochromes c; Down-Regulation; Exercise; Hepatitis; Humans; Interleukin-1beta; Intra-Abdominal Fat; Lipid Metabolism; Liver; Mitochondria; Non-alcoholic Fatty Liver Disease; Oxidative Stress; Reactive Oxygen Species; Sterol Regulatory Element Binding Protein 1; Tumor Necrosis Factor-alpha

<b>Background and Objective:</b> Hepatitis is a liver illness caused by a viral infection, autoimmune conditions or the use of certain medicines. In molecular hepatitis treatment, cytochrome c can be used as a potential predictor of the severity of liver impairment. In Asia, particularly in Indonesia, antioxidant-rich plants include <i>Ficus</i> <i>carica</i> and <i>Olea europaea.</i> This study aimed to see what impact cytochrome c in hepatitis after these two botanicals were administered. <b>Materials and Methods:</b> Rats were grouped as follows: Normal rats with no additions or herbs (G₀), the physiological solution group (G₁), the intravenous administration of the quercetin-copper (II) (G₂), Olive leaf extract or OLE (300 mg kg¹ b.wt.) (G₃) and Tin leaf extract or TLE (100 mg kg¹ b.wt.) (G₄). For an animal model of hepatitis, the rats were given thioacetamide 280 mg kg¹ b.wt., 8 days later. The rats were dissected and blood and liver samples were collected for enzyme and immunohistochemistry examination. <b>Results:</b> Malondialdehyde (MDA), superoxide dismutase (SOD) and cytochrome c expression levels differed significantly (p<0.05) across treatment groups in rat's models of hepatitis. Hepatocytes first displayed symptoms of lipid degradation, inflammatory and necrosis cells. When administered quercetin and the two herbs, necrosis and inflammatory cells were reduced, demonstrating that OLE and TLE can enhance liver histology and lower cytochrome c expression in a mouse model of hepatitis. <b>Conclusion:</b> Administration of Olive leaf extract (OLE) and Tin leaf extract (TLE) can improve liver histology in hepatitis model rats while decreasing cytochrome c expression, which is a mechanism for hepatocyte cell death.

Topics: Animals; Cytochromes c; Ethanol; Ficus; Hepatitis; Mice; Necrosis; Olea; Oxidative Stress; Plant Extracts; Quercetin; Rats

Topics: Amino Acids; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Cytochromes; Cytochromes c; Electrons; Hepatitis; Liver; Microscopy; Microscopy, Electron; Mitochondria; Mitochondrial Proteins; Rats; Research; Spectrum Analysis

Topics: Cytochromes; Cytochromes c; Electron Transport Complex IV; Enzyme Inhibitors; Hepatitis; Humans; Hyperbilirubinemia; Jaundice; Liver Diseases

Topics: Animals; Carbon Tetrachloride; Cytochromes c; Hepatitis; Ketoglutaric Acids; Rats; Sodium