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Study On The Mechanism Of Regulating Lipids And Protecting Liver By Genistein

Posted on:2016-07-02Degree:MasterType:Thesis
Country:ChinaCandidate:Y RongFull Text:PDF
GTID:2284330470984614Subject:Cell biology
Abstract/Summary:PDF Full Text Request
Genistein (Gen) is a common secondary metabolites of soybeans and other legumes, which are widely involved in regulation of various physiological activities of human lipid metabolism, glucose metabolism, anti-oxidation Hepatic steatosis and excessive deposition of fat in cells is the main feature of Nonaleoholie Fatty Liver Disease (NAFLD) which is one of the most common diseases of stress-induced liver injury now. Adipose Triglyceride Lipase (ATGL) is the rate-limiting enzyme lipolysis in latest discovery, the activation pathway of which are much different from other lipases.Objective:A variety of cells in vitro are used with experimental for steatosis modeLThe phenomenon of fat deposition is simulation to NAFLD. Gen adjusts the effect of steatosis model within Triglyceride (TG) and is the role in the regulation of ATGL processing. Gen controls the regulation of lipid metabolism by peroxisome proliferator activated receptor signaling pathways (PPAR). Studying the mechanism of regulating lip ids and protecting liver through the PPAR.Pre venting fatty liver by foods and discussing the pharmacological target of preventing NAFLD.Methods:Hep G2,Hep 3b, L-02 and 3T3-L1 cells was used as the experimental subjects.Experiment is divided into three parts. First, dose of oleic acid is using to induced intracellular fat deposition excessively. The intracellular TG content, morphological changes, cell viability, cell culture medium alanine aminotransferase (ALT) activity, cell culture medium aspartate aminotransferase (AST) activity and other biochemical markers are detected to studying the effect of cell steatosis inducing by OA. Establishing a appropriate cell steatosis models by combining all factors;Second, Gen processes steatosis cells,studying the cell morphology and intracellular TG changes.the lipid-lowering effect in steatosis cells is convinced;The third step, Gen treated with the steatosis cells, ATGL, HSL, PPARa, PPARymRNA expressions is measured by real-time quantitative PCR assay, PPARa, PPARy protein expression is measured by ELISA test measures. Studying the mechanism of regulation about TG by Gen.Results:(1) Different concentrations of OA could act on Hep G2, Hep 3b, L-02 and 3T3-L1 cells, thus producing intracellular fat accumulation phenomenon. Low concentration (concentration<1mM) of OA can induce low levels of fat accumulation, but cell supernatants enzyme index did not change significantly. High concentrations of OA (concentration> 1mM) changed enzymatic activity of the cell significantly, inducted cell death part. (2) Gen can significantly reduce the TG content of the cells. Reducing the amount of TG concentration, Gen significant dose-dependent manner. (3) Gen can increase PPARa, PPARy mRNA and protein express ion, the simultaneous increase on ATGL, HSL mRNA expression.Conclusion:1mM OA can induce a higher-quality model of steatosis cells. Gen can regulate the fat content of intracellular triglycerides, improve TG of cell metabolism. Gen increases ATGL, HSL lipase activity way through PPARs. Regulating lipid metabolism of lipid-lowering effects has important physiological significance.
Keywords/Search Tags:Genistein, Triglycerides, PPAR, ATGL, HSL
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