中国比较医学杂志2026，Vol.36Issue(1)：22-33,12.DOI:10.3969/j.issn.1671-7856.2026.01.003
康复新液抑制NF-κB通路及巨噬细胞M1型极化减轻IBD小鼠结肠炎的作用机制
Mechanism of colitis alleviation by inhibiting the nuclear factor-κB pathway and macrophage M1 polarization via Kangfuxin liquid in inflammatory bowel disease mice
摘要
Abstract
Objective The pathological mechanism of inflammatory bowel disease(IBD)is closely related to overactivation of the nuclear factor-κB(NF-κB)signaling pathway and M1 polarization of macrophages.Accordingly,this study aimed to investigate the effects of Kangfuxin solution on the regulatory mechanism of the NF-κB pathway during the progression of IBD.Methods A mouse model of IBD was established using dextran sodium sulfate(DSS).Forty-eight C57BL/6 mice were divided into eight groups:Control,Model,SASP,KFX-L(5 mL/kg),KFX-M(10 mL/kg),KFX-H(20 mL/kg),NF-κBi-pretreated and NF-κBi-pretreated+KFX-H groups.The disease activity index(DAI),colonic mucosal damage index(CMDI),and histopathological scores were recorded.mRNA expression levels of CD86,tumor necrosis factor-α(TNF-α),phosphorylated NF-κB inhibitor α(p-IκBα),and interleukin(IL)-1β in colonic tissues were detected by RT-qPCR,and protein expression levels of CD86,inducible nitric oxide synthase,and p-IκBα in colon tissues were detected by Western blot.Flow cytometry was used to analyze the effect of Kangfuxin liquid on the disease model.Results DSS-induction successfully established a mouse IBD model,with the measured values of various research indicators being highest in the Model group(P<0.05).The indicators in each group,except the SASP group,were significantly decreased compared with the Model group(P<0.05),while downregulation of CD86 in the SASP group was not significant(P>0.05).Among the three Kangfuxin liquid groups,the indicators were significantly reduced in the KFX-H group(P<0.05).The combined intervention of NF-κB inhibitor and high-dose Kangfuxin liquid did not significantly enhance the therapeutic effect,with no significant differences in the measured values of each indicator compared with the single-drug groups(P>0.05).Conclusions Kangfuxin liquid,sulfasalazine and NF-κB inhibitors all have protective effects on colonic inflammation in DSS-induced IBD model mice,but their sites of action differ.Kangfuxin liquid and NF-κB inhibitors synergistically attenuate the intestinal inflammatory response by inhibiting NF-κB pathway activation through reducing IκBα phosphorylation,as well as down-regulating macrophage M1-type polarization.In contrast,sulfasalazine exerts a weaker effect on macrophage M1 polarization.关键词
炎症性肠病/NF-κB通路/巨噬细胞极化/调控机制/康复新液Key words
inflammatory bowel disease/NF-κB signaling pathway/macrophage polarization/regulatory mechanism/Kangfuxin liquid分类
医药卫生引用本文复制引用
陈立,李捷,张杉杉,王宁,吴学东..康复新液抑制NF-κB通路及巨噬细胞M1型极化减轻IBD小鼠结肠炎的作用机制[J].中国比较医学杂志,2026,36(1):22-33,12.基金项目
云南省教育厅科学研究基金项目(2024Y894). （2024Y894）
