AIM The aim of the present study was to evaluate the effect of salvianolie acid A (SalA) on the pathological progression of hepatic fibrosis in rats with type 2 diabetes and investigate its liver-protective mechanism.METHODS After the animal model of hepatic fibrosis with type 2 diabetes was successfully made with high-sucrose, high-fat diet-fed and low-dose streptozotocin (STZ),SalA (0.3 mg·kg-1, i.g) was administered to diabetic rats for four months.The hepatic pathological progress and the expression of α-smooth-muscle-actin (ct-SMA) and transforming growth factor β1 (TGF-β1) in liver tissue were observed.Hepatocytes apoptosis and hepatic mitochondrial respiratory function were evaluated.RESULTS HE staining and Picro acid-Sirius red staining confirmed that SalA significantly alleviated the lesion of hepatic steatosis and fibrosis.The expressions of α-SMA and TGF-β1 in liver tissue were markedly reduced by immunohistochemistry staining.Terminal desoxynucleotide transferase-mediated dUTP nick end labeling staining showed that SalA reduced hepatocytes apaptosis.In addition, SalA improved the injured hepatic mitochondrial respiratory function.CONCLUSION The findings suggested that SalA could prevent the pathological progress of hepatic fibrosis in rats with type 2 diabetes.Its liver-protecting mechanism might be involved in reducing oxidative stress, further suppressing the expression of α-SMA and TGF-β1expression, also anti-apoptosis and mitoehondria-proteetive potential.