首页|期刊导航|中医临床研究|基于丝裂原活化蛋白激酶信号通路探讨黄芪多糖对肠上皮-巨噬细胞共培养肠炎模型的改善作用及机制

基于丝裂原活化蛋白激酶信号通路探讨黄芪多糖对肠上皮-巨噬细胞共培养肠炎模型的改善作用及机制OA

Exploring the therapeutic effect and mechanism of astragalus polysaccharides on intestinal epithelial cell-macrophage co-cultured enteritis model via the MAPK signaling pathway

中文摘要英文摘要

目的:研究黄芪多糖对人结直肠腺癌细胞(Caco-2)/巨噬细胞RAW264.7共培养肠炎模型中炎性反应的改善作用,并探讨其潜在机制.方法:将不同浓度的黄芪多糖(50 μg/mL、100 μg/mL)作用于脂多糖诱导的 Caco-2/RAW264.7 共培养肠炎模型,通过测定肠碱性磷酸酶(intestinal alkaline phosphatase,IAP)、二胺氧化酶(diamine oxidase,DAO)活性及紧密连接蛋白-1(zonula occludens-1,ZO-1)的表达评估黄芪多糖对肠道屏障功能损伤的保护作用,测定细胞炎症因子肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-1β(interleukin-1β,IL-1β)、白细胞介素-6(interleukin-6,IL-6)的水平及丝裂原活化蛋白激酶(mitogen activated protein kinase,MAPK)信号通路中细胞外信号调节激酶(extracellular signal-regulated protein kinase,ERK)和 p38 MAPK 蛋白磷酸化水平,探究黄芪多糖改善肠炎的潜在分子机制.结果:与模型组相比,黄芪多糖高剂量组(100 μg/mL)能显著提高 IAP、DAO 的活性(P<0.05);黄芪多糖高剂量组、黄芪多糖低剂量组(100 μg/mL、50 μg/mL)均能显著增加 ZO-1 蛋白的表达,并呈剂量依赖性(P<0.05).此外,黄芪多糖高剂量组能显著降低炎症因子 TNF-α、IL-1β、IL-6的分泌(P<0.05);黄芪多糖高剂量组、黄芪多糖低剂量组均能显著抑制MAPK 信号通路的激活,降低 ERK 和 p38 MAPK 蛋白磷酸化水平,从而有效抑制炎性反应(P<0.05).结论:黄芪多糖能通过抑制MAPK 信号通路减轻 Caco-2/RAW264.7 共培养肠炎模型的炎性反应,保护肠道屏障的完整性,为黄芪多糖在天然抗炎性反应食品和药品开发领域的应用提供理论基础.

Objective:To investigate the ameliorative effect of astragalus polysaccharide(APS)on the inflammatory response in the Caco-2/RAW264.7 co-culture intestinal model and explore its potential mechanism.Methods:Different concentrations of APS(50 μg/mL,100 μg/mL)were applied to the Caco-2/RAW264.7 co-culture intestinal inflammation model induced by Lipopolysaccharide(LPS).The protective effect of APS on intestinal barrier function damage was evaluated by measuring the activities of intestinal alkaline phosphatase(IAP)and diamine oxidase(DAO),and the expression of tight junction protein zonula occludens-1(ZO-1).Meanwhile,the potential molecular mechanism of APS in improving intestinal inflammation was explored by determining the levels of inflammatory cytokines(TNF-α,IL-1β,IL-6)and the phosphorylation levels of ERK and p38 MAPK proteins in the mitogen-activated protein kinase(MAPK)signaling pathway.Results:Compared with the model group,the activities of IAP and DAO in the high-dose group(100 μg/mL)were statistically significantly increased(P<0.05).The expression of ZO-1 protein in both the high-dose and low-dose groups(100 μg/mL,50 μg/mL)were statistically significantly increased in a dose-dependent manner(P<0.05).In addition,the secretion of inflammatory cytokines TNF-α,IL-1β,and IL-6 in the high-dose group were statistically significantly reduced(P<0.05).Both the high-dose and low-dose groups significantly inhibited the activation of the MAPK signaling pathway and decreased the phosphorylation levels of ERK and p38 MAPK proteins,thereby effectively suppressing the inflammatory response(P<0.05).Conclusion:APS can alleviate the inflammatory response in the intestinal co-culture model by inhibiting the MAPK signaling pathway and protect the integrity of the intestinal barrier,which provides a theoretical basis for the application of APS in the development of natural anti-inflammatory foods and drugs.

钟晞;慕嘉欣;许晓蕾;吴莉

江西中医药大学药学院,江西 南昌,330004江西中医药大学药学院,江西 南昌,330004江西中医药大学中医学院,江西 南昌,330004江西中医药大学药学院,江西 南昌,330004||江西中医药大学中医学院,江西 南昌,330004

医药卫生

黄芪多糖Caco-2/RAW264.7共培养肠炎模型肠道屏障炎症丝裂原活化蛋白激酶信号通路

Astragalus polysaccharideCaco-2/RAW264.7 cell co-culture modelIntestinal barrierInflammationMAPK signaling pathway

《中医临床研究》 2026 (1)

22-27,6

江西省卫生健康委科技计划(202211406)江西省研究生创新专项(YC2024-B220)江西中医药大学大学生创新创业训练计划(202410412155X、202410412149).

10.3969/j.issn.1674-7860.2026.01.003

评论