PPARα Activated Protects High-fat Diet Induced Nonalcoholic Fatty Liver Disease In Rats

Objective: non- alcoholic fatty liver disease is the cause of chronic liver disease, the most common cause of abnormal liver function one can evolve with the progression of the disease is non-alcoholic steatohepatitis, the eventual development of liver fibrosis, primary liver cancer. With the improvement of living standards, the impact of non-alcoholic fatty liver disease is becoming increasingly important for health. Hhis experiment aims to build high-fat diet-induced rat model nonalcoholic fatty liver disease, to study the protective effect and mechanism of PPARα agonist WY14643 affected on high-fat diet induced non-alcoholic fatty liver disease in rats.Methods: High-fat diet-induced rat model of nonalcoholic fatty liver disease, research was divided into two parts, the first part: the use of high-fat diet-induced occurrence of nonalcoholic fatty liver disease in rats. 4-week-old SPF SD male rats were randomly divided into three groups: Group I:control group(control), a standard diet. Group II: high-fat diet. Group III: high-fat diet, while intraperitoneal injection WY14643 1 mg/(kg*d). Rats were killed in the experimental of the first four weeks, to use HE staining of liver histopathology. The second Part: PPARα agonist WY14643 made PPARα gene was highly expressed in rat liver cells to study the effects of rat PPARα gene nonalcoholic fatty liver disease. 4-week-old SPF SD male rats were randomly divided into three groups: Group I:control group(control), a standard diet. Group II: high-fat diet. Group III: high-fat diet, while intraperitoneal injection WY14643 1 mg/(kg*d). Rats were killed in the experimental of the first four weeks, we used RT-PCR and Western blot to analyze the expression of PPARα、Besp m RNA and protein. and detected serum biochemical marks of TBA、TG、TC、AST、ALT.Results: the first part: high-fat diet induced model of non-alcoholic fatty liver disease After HE staining of liver tissue under a microscope to change, Group I in rat liver lobule structure intact, Group II showed varying degrees of liver cell degeneration, fatty degeneration of the more obvious, Group III rat liver cell degeneration and necrosis, steatosis and inflammatory cell infiltration and comparison Group II were all reduced.Conclusion: High-fat diet could lead to the occurrence of non-alcoholic fatty liver disease in rats, liver cell degeneration and necrosis, fatty degeneration and inflammatory cell infiltration. Conclusion PPARα agonist WY14643 could regulate bile acid and lipid metabolism by increasing the expression of Besp and protect high-fat diet induced non-alcoholic fatty liver disease in rats.