基于网络药理学与分子对接技术探讨芪茵颗粒治疗非酒精性脂肪肝的机制研究OA

Objective:To predict potential targets and signaling pathways of Qiyin Keli(QYKL)against nonalcoholic fatty liv-er disease(NAFLD)using network pharmacology and molecular docking,and to investigate its underlying mechanism in NAFLD rats.Methods:Candidate targets and key pathways associated with QYKL in NAFLD treatment were predicted using network pharmacology and molecular docking.Sprague-Dawley rats were randomly assigned to a normal control group and a mod-el group,in which the NAFLD model was induced by high-fat diet feeding.After successful modeling,the NAFLD rats were fur-ther randomized into five subgroups:model(HF)group,low-dose QYKL(HF+L)group,medium-dose QYKL(HF+M)group,high-dose QYKL(HF+H)group,and metformin plus tiopronin treatment(HF+MT)group.All rats were fed for 13 consecutive weeks,and corresponding interventions were administered by intragastric gavage for 30 days.Hepatic pathological changes were examined by H&E staining and transmission electron microscopy.Serum triglyceride levels were determined to eval-uate hepatic steatosis.Serum inflammatory cytokines were measured by ELISA,and hepatic inflammatory protein expression was detected by immunohistochemistry.Results:A total of 107 active ingredients were identified from QYKL,with AKT1,TNF-α,IL-6 and IL-1β as core gene targets.The PI3K-AKT signaling pathway was recognized as a crucial pathway mediating the anti-NAFLD effects of QYKL.Animal experiments showed marked hepatic steatosis in the HF group,along with nuclear pyknosis and abundant intracellular lipid droplets under electron microscopy.Compared to the HF group,hepatic steatosis was significantly ameliorated in the HF+M group(P<0.01),accompanied by normalized serum triglyceride levels.ELISA revealed that TNF-α,IL-6 and IL-1β levels were prominently reduced in the HF+M group(P<0.01).Immunohistochemical results confirmed that the expression of TNF-α and IL-6 was significantly elevated in the HF group(P<0.01)but distinctly decreased in the HF+M group(P<0.01).Conclusion:Qiyin Keli may alleviate hepatic pathological injury in NAFLD rats by modulating inflammation and insu-lin resistance through the PI3K-AKT signaling pathway.