四白汤对乙醇诱导下小鼠胃溃疡的防治作用研究OACSTPCD

[Objective]This study aims to investigate the prophylactic and therapeutic effects of Sibai Decoction(SBT)on gastric ulcers(GU)induced by ethanol(EtOH)in mice,and to explore its underlying molecular mechanisms,thus providing a theoretical basis for its clinical application in treating GU.[Methods]In vitro,five groups of mice were administered with high,medium,and low doses of SBT for 7 days,after which blood was collected to separate serum for the establishment of a serological research model.Human gastric epithelial cells(GES-1)were cultured in media containing drug-serum and treated with 0.8 mol/L EtOH for 4 hours after entering the G0 phase to establish a GES-1 cell injury model.Cell viability and the effects of SBT-containing serum on cell proliferation were measured using the Cell Counting Kit-8(CCK8)method.In vivo,60 mice were divided into six groups evenly and pre-treated with SBT before EtOH induction to develop a gastric mucosal injury model.The effects of SBT on the mouse weight and food intake were observed.Histopathological changes in the gastric mucosa were assessed by Hematoxylin and Eosin(HE)staining.Levels of inflammatory markers,including Interleukin 6(IL-6),Interleukin 1 Beta(IL-1 β),Tumor Necrosis Factor Alpha(TNF-α),and Interleukin 10(IL-10)protein expression levels,were measured in the serum using Enzyme-Linked Immunosorbent Assay(ELISA).Gastric mucosal levels of Malondialdehyde(MDA),Reactive Oxygen Species(ROS),Glutathione Peroxidase(GSH-Px),and Nitric Oxide(NO)were assessed using biochemical kits.The expression of proteins involved in the PI3K/AKT/NF-κB pathway,including Phosphorylated Phosphatidylinositol 3-Kinase(P-PI3K),Phosphorylated Protein Kinase B(P-AKT),Phosphorylated Nuclear factor kappa-B inhibitor alpha(P-IκBα),Nuclear Nuclear Factor Kappa B p65(Nuclear NF-κB p65),and Cytoplasmic Nuclear Factor Kappa B p65(Cytoplasm NF-κB p65),were analyzed by Western blot.[Results]In vitro experiments demonstrated that SBT significantly promoted the proliferation of EtOH-damaged GES-1 cells,with no apparent toxicity,and notably improved cell viability in the presence of EtOH.In vivo results indicated that SBT pre-treatment significantly ameliorated the body weight(P＜0.05)and food intake(P＜0.05)in the EtOH-induced GU model in mice;reduced histopathological damage;decreased serum levels of inflammatory markers IL-iβ(P＜0.01),TNF-α(P＜0.01)and IL-6(P＜0.01),and increased IL-10 expression(P＜0.01);lowered ROS levels(P＜0.01)and increased GSH-Px levels(P＜0.01)in the gastric mucosa,while effects on MDA and NO were not significant;significantly decreased the relative protein expression of P-P13K/PI3K(P＜0.01),P-AKT/AKT(P＜0.01)and Nuclear NF-κB p65/Cytoplasm NF-κB p65(P＜0.01),and significantly increased P-IκBα/IκBαexpression(P＜0.01).[Conclusion]SBT exhibits significant prophylactic and therapeutic effects on EtOH-induced GU in mice by enhancing antioxidative stress capacity,mitigating inflammatory responses,and regulating the PI3K/AKT/NF-κB pathway,providing a theoretical foundation for the further development and application of SBT in treating GU.