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Objective: To observe the willow tea extract on rats with nonalcoholic fatty liver disease liver function, antioxidant capacity and morphological structural damage, and to explore its key enzymes and liver fat metabolism relationship between gene expression and clear peroxidation the way in which argumentation Willow Tea on non-alcoholic fatty liver disease in rat liver protective effect of the possible mechanisms for the clinical application of drug efficacy and safety provide a theoretical basis. Methods: SD rats high-fat diet for six weeks, to replicate the model of non-alcoholic fatty liver disease after the animals were randomly divided into four groups, each with saline and willow tea extract low, medium and high doses of aqueous gavage 8 weeks after death. Ordinary diet for the same period in SD rats 6 weeks, normal saline were sacrificed after 8 weeks as normal controls. Automatic biochemical analyzer in serum ALT, AST, TG, CHOL, LDL and HDL levels and liver homogenates TG, CHOL content; produce liver biopsy, morphological changes observed under light microscope; by RT-PCR and SYBR Green real-time PCR assay PPARa key enzyme in the liver fat metabolism and its downstream ACO, LCAD, CYP4A1 and antioxidant enzyme CAT, GSH-Px mRNA relative expression levels; Western Blot assay core gene PPARα protein expression levels. Results: Compared with non-alcoholic fatty liver disease model group, willow tea extract low, medium dose group ALT levels decreased, the difference was statistically significant (P lt; 0.05); AST levels decreased (low dose group P lt; 0.05 , middle dose group P lt; 0.01). Liu tea extract dose group liver homogenate CHOL, TG content decreased, the difference was statistically significant (respectively P lt; 0.01, P lt; 0.05); low and high dose group content decreased liver homogenate CHOL (P lt; 0.05). Liu tea extract each dose group, serum CHOL, TG levels decreased, HDL levels, the difference was statistically significant (P lt; 0.05). Liver biopsy showed Liu tea each dose group to reduce hepatic steatosis, cell edema, necrosis improved to some extent. PCR results are shown willow tea extract, high dose group PPARαmRNA expression increased significantly (P lt; 0.01); ACO mRNA expression was increased, the difference was statistically significant (low-dose group P lt; 0.05, medium and high dose group P lt; 0.01); LCAD mRNA expression increased, low, medium dose group difference was statistically significant (low-dose group P lt; 0.05, middle dose group P lt; 0.01); CYP4A1 mRNA expression was increased, the difference was statistically significance (medium dose group P lt; 0.05, high dose group P lt; 0.01). Compared with model group, willow tea extract low, medium and high dose groups antioxidant enzymes CAT mRNA expression was increased, the difference was statistically significant (respectively P lt; 0.05, P lt; 0.01, P lt; 0.05); Low , middle dose group GSH-Px mRNA expression increased, the difference was statistically significant (respectively P lt; 0.05, P lt; 0.01). Western Blot (?) Core enzyme shows the results from the Willow Tea PPARα protein low-dose group to the high dose group increased accordingly. Conclusion: willow tea extract can repair non-alcoholic fatty liver disease and liver function damage liver tissue damage, and promote liver cell fat metabolism rate and antioxidant capacity. Its protective effect on the liver fat metabolism by regulating the key enzyme in the liver PPARα and its downstream target genes ACO, LCAD, CYP4A1 and CAT, GSH-Px in the gene or protein level to achieve.
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