【摘要】 目的 观察木兰花碱对溃疡性结肠炎（UC）大鼠核因子（NF）-κB信号通路和Nod样受体家族含pyrin结构域蛋白3 （NLRP3）炎性小体活性的影响，探讨木兰花碱对UC的作用及其机制。方法 SD大鼠60只，随机分为正常对照组、模型对照组、5-氨基水杨酸组(100 mg·kg^-1)和木兰花碱小、中、大剂量组(25,50,100 mg·kg^-1),每组10只。正常对照组灌胃纯净水，其余5组灌胃给予相应药物，每天1次，连续10 d。给药结束后，取结肠组织，经苏木精-伊红（HE）染色后观察组织结构；酶联免疫吸附实验（ELISA）法检测结肠组织中促炎症细胞因子白细胞介素（IL）-1β、IL-18和肿瘤坏死因子（TNF）-α含量；免疫荧光法检测CD11b⁺巨噬细胞数量；蛋白免疫印迹法和免疫组织化学法检测木兰花碱对NF-κB/NLRP3炎性小体信号通路相关蛋白的影响。结果 木兰花碱可降低UC大鼠的疾病活动指数、病理组织学评分、促炎症细胞因子表达水平和结肠组织中CD11b⁺巨噬细胞数量。木兰花碱降低UC大鼠结肠组织中p-IκBα、p-IKKβ和细胞核p-NF-κB p65蛋白表达水平，增加细胞质p-NF-κB p65蛋白表达水平。木兰花碱明显降低NLRP3炎性小体相关蛋白（NLRP3、ASC、cleaved caspase-1）的表达水平。结论 木兰花碱对UC模型大鼠有明显治疗作用，其机制可能与调控NF-κB/NLRP3炎性小体信号通路密切相关。更多还原

【Abstract】 Objective To observe the effect of magnoflorine on NF-κB signaling pathway and NLRP3 inflammasome activity, and to explore the possible mechanism of magnoflorine on ulcerative colitis in rats. Methods Sixty SD rats were randomly divided into normal control group, model control group, 5-aminosalicylic acid group(100 mg·kg^-1) and magnoflorine low-dose, medium-dose and high-dose groups(25,50,100 mg·kg^-1),with 10 rats in each group.The normal control group was given purified water by gavage, and the other 5 groups were given corresponding drugs by gavage, once a day for 10 days.After the administration, the colonic tissue of rats was collected, stained by hematoxylin and eosin（HE） and observed under microscope.The contents of pro-inflammatory cytokines（IL-1β,IL-18 and TNF-α） in colon tissues were detected by the ELISA method.The number of CD11 b⁺ macrophages was detected by the immunofluorescence method.The effect of magnoflorine on the express of NF-κB/NLRP3 inflammasome signaling pathway related protein was detected by western blotting and immunohistochemistry method. Results Magnoflorine could reduce the disease activity index, histopathological score, the expression levels of pro-inflammatory cytokines and the number of CD11 b⁺ macrophages in colon tissue of UC rats.Magnoflorine decreased the expressions of p-IκBα and p-IKKβ protein in the colon tissue of UC rats and p-NF-κB p65 protein in the cell nucleus, and increased the expression of p-NF-κB p65 protein in the cytoplasm.Magnoflorine significantly decreased the levels of NLRP3 inflammasome-related proteins（NLRP3,ASC,Cleaved caspase-1）. Conclusion Magnoflorine has an obvious therapeutic effect on the rats with UC,the mechanism of which may be closely related to the regulation of NF-κB/NLRP3 inflammasome signaling pathway.更多还原