RESUMEN
Aim To study the regulatory effect of FOXA2 on liver function and blood lipid levels in mice with intrahepatic cholestasis and hyperlipidemia. Methods The model was constructed by feeding high cholesterol/cholic acid (CAD), and the FOXA2 plasmid was injected into the liver of mice by tail vein hypertension, so that the hepatocytes overexpressed F0XA2. The automatic blood biochemical analyzer was uses to detect the blood biochemical indicators of the serum, the colorimetric method to detect the cholesterol level in liver, and ELISA method to detect the liver bile acid level. Western blot was used to determine the expression of liver FOXA2, and RT-PCR to assess the mRNA expression of genes related to bile acid metabolism. H&E and oil red staining were employed to observe liver pathology. Results With the extension feeding time of the CAD, the weight of the mice continued to decrease (P < 0.01), the gallbladder increased significantly (P < 0.01), and the level of transaminase increased, and serum cholesterol and low-density lipoprotein cholesterol (P < 0.01) increased significantly. Liver tissue structure was damaged, liver cholesterol was elevated (P <0.01), bile acid level increased (P < 0.01), and lipid accumulation was serious. Overexpression of FOXA2 could significantly improve liver function and dyslipidemia in CAD-fed mice by regulating liver bile acid metabolism genes, and reduce liver bile acid levels (P < 0.01) and liver lipid accumulation. Conclusions FOXA2 improves liver function and blood lipid levels in mice with intrahepatic cholestasis and hyperlipidemia.