Shengjiang Powder alleviates oxidative stress damage and fibrosis in mice with atherosclerosis concurrent with non-alcoholic fatty liver disease.

OBJECTIVE: To investigate the effects of "Shengjiang Powder", a representative formula for "simultaneous treatment of liver and heart," on liver tissue inflammation and fibrosis in mice with atherosclerosis(AS) concurrent with non-alcoholic fatty liver disease (NAFLD). METHODS: Ten wild-type male C57/B6J mice were assigned to the control group, and 40 ApoE -/- mouse were randomly divided into the model group, atorvastatin group, and traditional Chinese medicine (TCM) treatment groups. The model group, atorvastatin group, and TCM treatment groups were fed a high-fat Western diet for 12 weeks. Atorvastatin and TCM groups were administered via gavage, while the control group and model group received sterile purified water via gavage for 12 weeks. Serum levels of ALT, AST, TRIG, TC, LDL, as well as liver tissue levels of SOD, MDA, and GSH were measured. HE staining was used to evaluate liver tissue morphology and inflammatory infiltration. Western blot was used to detect the effect of Shengjiang Powder on the activation of AMPK/mTOR signaling pathway. Network pharmacology analysis was performed beforehand to identify potential targets of Shengjiang Powder in regulating fatty liver and atherosclerosis, with AMPK identified as a key target. RESULTS: Compared with the model group, the Shengjiang Powder treatment reduced serum levels of TRIG, TC, and LDL (P < 0.05), increased liver SOD and GSH activity (P < 0.01), decreased MDA (P < 0.01), alleviated liver steatosis, reduces the area of aortic sinus plaques, improved hepatic steatosis and inflammation, inhibited the expression of inflammatory factors and activated the AMPK/mTOR signaling pathway, consistent with the network pharmacology prediction that AMPK is a critical regulatory target. CONCLUSION: Treatment with "Shengjiang Powder," a representative formula for "simultaneous treatment of liver and heart," can slow the progression of atherosclerosis and concurrent NAFLD. The dosage shows a positive correlation with efficacy, and this effect is related to the regulation of liver oxidative stress and inflammation-induced fibrosis pathways.