The Role of Wnt/beta-Catenin Signal Pathway in the Pathogenesis of Nonalcoholic Fatty Liver Disease and the Effect of Atorvastatin Intervention

Abstract

The purpose of this study was to analyze the pathogenesis of nonalcoholic fatty liver disease in rats and study the efficacy of atorvastatin intervention. One hundred Sprague Dawley rats were selected as test system. These rats were randomly divided into 5 groups, the control group, the nonalcoholic fatty liver disease group, high-dose atorvastatin group, medium-dose atorvastatin group and low-dose atorvastatin group, each containing 20 animals. An equal dose of sodium carboxymethylcellulose was applied to the model group and the control group; while atorvastatin perfusion was given to the other 3 groups. The levels of serum aspartate aminotransferase, alanine aminotransferase, triglycerides, total cholesterol, high-density lipoprotein, low-density lipoprotein and malondialdehyde were compared among the groups. The serum levels of aspartate aminotransferase, alanine aminotransferase, triacylglycerol and total cholesterol of the high-fat diet model group were significantly higher; moreover, the expression levels of MMP2, MMP9, Wnt1, Wnt4, host-catenin were significantly elevated. Treatment with atorvastatin could effectively ameliorate this abnormal condition but at high doses. Atorvastatin appears to inhibit the Wnt/β-catenin signal pathway and achieve good curative effect against nonalcoholic fatty liver disease.