The global incidence of
nonalcoholic fatty liver disease (
NAFLD) is increasing. The present study explored the effect and mechanism of
berberine (BBR) on
NAFLD in rats. Thirty-five Sprague-Dawley rats were randomly divided into the control and
NAFLD groups, which were fed a normal diet or high-fat diet, respectively, for 8 weeks.
Hematoxylin and
eosin staining was performed on liver tissues and establishment of the
NAFLD model was confirmed by microscopy.
NAFLD rats were subsequently randomly subdivided and treated with saline or BBR for 8 weeks. The liver wet weight of rats in each group was measured, the liver tissue structure was observed by microscopy, and
alanine aminotransferase (ALT),
aspartate aminotransferase (AST), total
cholesterol (TC),
triglyceride (TG), fasting
blood glucose (FBG),
low-density lipoprotein (
LDL) and
high-density lipoprotein (HDL) levels were detected using a semi-automatic biochemical detector. Reverse transcription-quantitative PCR and western blotting were performed to determine the
mRNA and
protein expression levels of
microsomal triglyceride transfer protein (
MTTP),
apolipoprotein B and
low-density lipoprotein receptor (LDLR). Compared with the control group, the liver wet weight of the
NAFLD rats was higher; the liver showed obvious fatty degeneration and liver TG levels increased significantly, as did serum levels of ALT, AST, TC, TG, FBG, HDL and
LDL, while expression of
MTTP and LDLR significantly decreased. Compared with the saline-treated
NAFLD rats, the BBR-treated rats had reduced liver wet weight, improved
liver steatosis and a significant decrease in liver TG levels, while ALT, AST, TC, TG, and
LDL serum levels significantly decreased and
MTTP levels were significantly upregulated. In conclusion, BBR treatment ameliorated the
fatty liver induced by a high-fat diet in rats. Furthermore, BBR reversed the abnormal expression of
MTTP and LDLR in rats with high-fat diet induced-
NAFLD. The present findings suggest that
fatty liver could be improved by BBR administration, via reversing the abnormal expression of
MTTP and LDLR and inhibiting
lipid synthesis.