Abstract:A hyperlipidemia rat model was used to explore the mechanism by which Shanxi aged vinegar reduces liver injury induced by a high-fat diet. The model involved intragastric administration of high-fat emulsion to rats for 5 weeks, whereas low, medium, and high doses (1.35, 2.7, 5.4 g/kg by body weight) of Shanxi aged vinegar were administered to the rats by gavage for 10 weeks. Serum total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), superoxide dismutase (SOD), glutathione reductase (GRx), total antioxidant capacity (T-AOC), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALK-P) levels were determined by serological testing. Pathological changes in the rat livers were examined using hematoxylin and eosin (H&E) staining. The mRNA and protein levels of JAK2 and STAT3 in the livers were detected using q-PCR and WB and immunohistochemical techniques were used for localization analysis.The results showed that Shanxi aged vinegar significantly reduced the serum lipid content and extent of liver injury in rats fed a high-fat diet (P<0.01), increased the activity of antioxidant enzymes, and significantly inhibited mRNA and protein levels of JAK2 and STAT3 in the rats (P<0.01). More specifically, serum TC and TG in the high-dose group was decreased by 20.50% and 48.65%, respectively, compared to the low-dose group. The high-dose and medium-dose groups showed the largest effects on AST (32.79% and 29.07%), ALT (21.65% and 20.67%) and ALK-P (19.42% and 19.71%). Compared with the low-dose group, the high-dose group had significantly lower mRNA levels of JAK2 (57.07%, 34.02%) and STAT3 (55.19%, 41.45%), and significantly lower protein levels of JAK2 (27.89%, 24.09%) and STAT3 (33.06%, 26.64%) (P<0.05, P<0.01, respectively). In conclusion, Shanxi aged vinegar attenuated liver injury induced by a high-fat diet in rats, and this may be achieved through inhibition of activation of the JAK2/STAT3 pathway.
