Exploration of the Mechanism of Qutan Huoxue Fang in Treating Non-alcoholic Fatty Liver Disease Based on the FXR-Srebp1c-FAS Pathway and CD36
Objective Farnesoid X receptor(FXR)-sterol regulatory element-bindingprotein-1c(Srebp1c)-fatty acid synthase(FAS)pathway related to endogenous fatty acid synthesis and CD36 related to exogenous intake of fatty acids were taken as the starting point to explore the molecular mechanism of Qutan Huoxue Fang against NAFLD.Methods Male C57BL/6J mice were divided into control group,model group,Qutan Huoxue Fang group,and Yishanfu group,10 mice in each group.The model group,Qutan Huoxue Fang group and Yishanfu group were fed with high-fat diet.After 4 weeks of administration,Qutan Huoxue Fang group and Yishanfu group began to give drug intervention.After 8 weeks of intervention,serum was collected for biochemical detection and liver tissues were used to detect pathology,total cholesterol(TC)and total triglyceride(TG)content of liver,FXR,Srebp-1c,FAS,CD36 gene and protein expression.Results Compared with the control group,the body mass and liver mass of mice in the model group were significantly increased(P<0.05).The results of liver pathology and the contents of TC and TG were increased(P<0.01),suggesting significant steatosis.The mRNA expression levels of FXR,Srebp1c and mRNA and protein expression of CD36 in liver tissue were significantly increased(P<0.01),FAS protein expression was decreased(P<0.05).Compared with the model group,body mass and liver mass of mice in Qutan Huoxue Fang group were significantly decreased(P<0.01).Hepatic steatosis was significantly reduced.The expressions of FXR mRNA in liver tissues were significantly increased(P<0.01),while the expression of Srebp1c,FAS,CD36 mRNA and protein(P<0.05)were significantly decreased.Conclusion Increased intake of exogenous fatty acids might be the main cause of NAFLD induced by high-fat diet.Qutan Huoxue Fang not only inhibited exogenous fatty acid intake,but also reduced endogenous fatty acid synthesis,and improved NAFLD by bidirectional regulation.
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