Effects Of Sanghuang On Nonalcoholic Fatty Liver Disease Induced By PCBs

Sanghuang belongs to Agaricomycotina,Agaricomycetes,Hymenochaetales.It’s a perennial fungus that lives on the trunk of mulberry trees.In recent years,sanghuang has been found and confirmed to have highly effective anti-tumor,anti-oxidation and lipid-lowering effects.Non-alcoholic fatty liver disease（NAFLD）is a clinicopathological syndrome caused by non-alcoholic factors or other liver damaging factors,and characterized by excessive accumulation of lipids in liver cells,which has become one of the main causes of liver transplantation at present.Polychlorinated biphenyls（PCBs）,as a typical type of Persistent organic pollutant（POPs）,is characterized by persistence,bioaccumulation,semi-volatility and high toxicity,it has become the focus of environmental protection.Recent studies have shown that PCBs exposure positively correlated with NAFLD.On this basis,we selected human normal hepatocyte WRL68 cell line as the in vitro experiment object,and systematically discussed the effect of ethanol sanghuang Kangneng（ESK）on high-fat WRL68 cells and metabolic disorder WRL68 cells induced by PCB156 exposure and its related molecular mechanism with means of molecular biology technology.The research results are as follows.（1）The content of flavonoids in ESK was determined by Na NO₂-Al（NO₃）₃colorimetric method 76.14%,and the content of polyphenol flavonoids in ESK was determined by HPLC,including quercetin,gallic acid,caffeic acid,icariin,rutin and chlorogenic acid.（2）In the model experiment of high-fat WRL68 cells treated with ESK,the results showed that the intracellular lipid content of high-fat WRL68 cells decreased significantly with the increase of ESK concentration.q RT-PCR showed that ESK exposure could significantly affect the expression of genes related to lipid metabolism in high-fat WRL68cells.Specifically,ESK could inhibit lipid synthesis by inhibiting the expression of Srebp-1c and Fas genes;By increasing intracellular PPARαgene expression,promote fatty acid oxidation.（3）The results showed that ESK significantly improve lipid accumulation and oxidative stress in hepatocytes induced by PCB156（3.4μM）.In addition,q RT-PCR results showed that ESK treatment significantly improved the expression of genes related to PCB156 and lipid metabolism（lipid transport,lipid production and lipid oxidation）and inflammatory factors.In summary,we confirmed that ESK can improve the formation of lipid metabolism disorders in liver cells induced by FFA or PCB156 exposure in vitro.In addition,ESK can improve the expression of oxidative stress and inflammatory factors in lipid metabolism disorders.In addition,in vivo studies have shown that PCB156 exposure can cause liver injury.