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目的:探讨白藜芦醇(RES)对葡聚糖硫酸钠盐(DSS)诱导溃疡性结肠炎(UC)小鼠的治疗效果，及其对Toll样受体4(TLR4)/髓样分化因子88(MYD88)/核转录因子-κB(NF-κB)信号通路的调控机制。方法:将90只BALB/c小鼠的体重通过SPSS生成随机数后，参照其大小排序分为对照(CON)组、模型(DSS)组、白藜芦醇低(RES-L，10 mg/kg)、中(RES-M，50 mg/kg)、高(RES-H，100 mg/kg)剂量组、柳氮磺砒啶(SASP)组。记录小鼠状况，测算疾病活动指数(DAI)，实时荧光定量聚合酶链式反应(RT-PCR)和蛋白免疫印迹法(Western blot)检测结肠上皮组织中TLR4、MYD88、NF-κB p65 mRNA和蛋白的表达；酶联免疫吸附法(ELISA)检测小鼠结肠肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)、白细胞介素-10(IL-10)的含量，并用Graph Pad Prism 8统计软件分析。结果:DSS组TLR4、MYD88、NF-κB p65显著高于CON组(0.315±0.046比0.082±0.011、0.279±0.025比0.085±0.012、0.244±0.026比0.052±0.011，n t＝8.352、12.045、11.476，n P<0.05)，差异有统计学意义，RES-H的TLR4、MYD88、NF-κB p65显著低于DSS组(0.105±0.016比0.311±0.045、0.094±0.012比0.295±0.021、0.103±0.015比0.245±0.026，n t＝9.174、7.285、11.163，n P<0.05)，差异有统计学意义；RES-H组TNF-α、IL-1β、IL-6显著低于DSS组(154.105±6.184比303.408±31.209、93.522±7.271比306.305±40.926、140.509±2.795比263.705±11.116，n t＝8.174、8.865、18.622，n P<0.05)，差异有统计学意义，RES-H组IL-10高于DSS组(110.708±4.154比93.846±3.232，n t＝5.565，n P<0.05)，差异有统计学意义。n 结论:RES通过调节TLR4/MYD88/NF-κB p65信号通路活化达到治疗UC的目的。“,”Objective:To study the therapeutic efficacy of resveratrol (RES) for dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) in mice and its regulatory effect on Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-κB (NF-κB) signaling pathway.Methods:After the weights of 90 BALB/c mice were randomly generated by SPSS, the mice were sorted according to their size and divided into control (CON) group and model (DSS) group according to their body weight, with low resveratrol (RES-L, 10 mg/kg), medium (RES-M, 50 mg) /kg), high (RES-H, 100 mg/kg) dose group, sulfasalazine (SASP) group. Status of mice was recorded, and disease activity index (DAI) was measured. The real-time fluorescent quantitative polymerase chain reaction (Real-time PCR) and Western blotting used to detect the expression of TLR4, MYD88 and NF-κB p65 mRNA and protein in colonic epithelial tissues respectively. The enzyme-linked immunosorbent assay (ELISA) was used to detect colonic tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-1β and IL-10 contents. GraphPad Prism 8 statistical software was used.Results:The expression of TLR4, MYD88, and NF-κB p65 in the DSS group was significantly higher than that in the CON group (0.315±0.046 vs. 0.082±0.011, 0.279±0.025 vs. 0.085±0.012, 0.244±0.026 vs. 0.052±0.011,n t=8.352, n t=12.045, n t=11.476, n P<0.05). The expression of TLR4, MYD88 and NF-κB p65 in the RES-H group was significantly lower than in the DSS group (0.105±0.016 vs. 0.311±0.045, 0.094±0.012 vs. 0.295±0.021, 0.103±0.015 vs. 0.245±0.026,n t=7.285, n t=11.163, n t=9.174, n P<0.05). TNF-α, IL-1β and IL-6 levels in the RES-H group were significantly lower than those in the DSS group (154.105±6.184 vs. 303.408±31.209, 93.522±7.271 vs. 306.305±40.926, 140.509±2.795 vs. 263.705±11.116,n t=8.174, n t=8.865, n t=18.622, n P<0.05). The IL-10 level in the RES-H group was significantly higher than that in the DSS group (110.708±4.154 vs. 93.846±3.232,n t=5.565, n P<0.05).n Conclusion:RES can treat UC by regulating the activation of TLR4/MYD88/NF-κB p65 signaling pathway.