目的 探讨白术内酯Ⅲ是否通过调节自噬水平清除过氧化物减轻小鼠溃疡性结肠炎（UC）。方法 将32只健康雄性BALB/c小鼠随机分为空白组（n=8）和造模组（n=24），造模组小鼠均采用2，4，6-三硝基苯磺酸（TNBS）/乙醇诱导造UC小鼠模型，造模成功后小鼠随机分为模型组、白术内酯Ⅲ组（20 mg·kg^-1）、白术内酯Ⅲ+自噬抑制剂组（20 mg·kg^-1+2 mg·kg^-1），造模成功后第2天起按相应剂量给药，连续给药14天。进行小鼠疾病活动指数（Disease activity index，DAI）及结肠黏膜损伤指数（Colonic mucosal damage index，CMDI）评分；测量小鼠结肠长度及重量；苏木精-伊红（Hematoxylin-eosin，HE）染色观察结肠组织病理学变化；酶联免疫吸附（Enzyme-linked immunosorbent assay，ELISA）检测结肠组织超氧化物歧化酶（Superoxidedismutase，SOD）、谷胱甘肽过氧化物酶（Glutathioneperoxidase，GSH-PX）、丙二醛（Malondialdehyde，MDA）含量；蛋白质免疫印迹（Western Blot，WB）检测结肠组织Beclin-1、LC3Ⅱ/Ⅰ、p62蛋白表达；透射电镜观察结肠上皮细胞中的自噬泡。结果 与空白组比较，模型组小鼠DAI、CMDI评分、单位结肠重量、结肠组织MDA含量及p62蛋白表达明显升高（P<0.05），小鼠结肠长度明显缩短、结肠组织SOD、GSH-PX含量及Beclin-1、LC3Ⅱ/LC3Ⅰ蛋白表达明显降低（P<0.05）。与模型组比较，白术内酯Ⅲ组小鼠DAI、CMDI评分、单位结肠重量、结肠组织MDA含量及p62蛋白表达明显降低（P<0.05），小鼠结肠长度、结肠组织SOD、GSH-PX含量及Beclin-1、LC3Ⅱ/LC3Ⅰ蛋白表达明显升高（P<0.05）。自噬抑制剂阻止白术内酯Ⅲ诱导的Beclin-1、LC3Ⅱ/LC3Ⅰ蛋白表达升高，抑制结肠组织SOD、GSH-PX含量。结论 白术内酯Ⅲ可明显改善UC病理损伤，通过调节自噬水平清除过氧化物发挥对UC小鼠的治疗作用。

Methods Thirty-two healthy male BALB/c mice were randomly divided into control group (n=8) and modeling group (n=24), and the mice in the modeling group were induced with 2,4,6-trinitrobenzenesulfonic acid (TNBS)/ethanol to create a UC mouse model. After successful modeling, the mice were randomly divided into model group, Atractylenolide III group (20 mg·kg^-1) and Atractylenolide III + autophagy inhibitor group (20 mg·kg^-1+2 mg·kg^-1), and administered at the corresponding doses for 14 d after successful modeling. The disease activity index (DAI) and colonic mucosal damage index (CMDI) scores of mice were observed; the length and weight of mouse colon were measured; the histopathological changes of colon were observed by Hematoxylin-eosin staining; the Superoxidedismutase, Glutathioneperoxidase and Malondialdehyde contents of colon tissues were detected by Enzyme-linked immunosorbent assay; the expression of Beclin-1, LC3II/Ⅰ and p62 protein in colon tissues were detected by Western Blot; the autophagic vesicles in colon epithelial cells were observed by transmission electron microscopy.Results Compared with the control group, the DAI, CMDI score, unit colon weight, colon tissue MDA content and p62 protein expression were significantly higher in the model group (P<0.05), and the colon length, colon tissue SOD, GSH-PX content and Beclin-1, LC3II/LC3Ⅰ protein expression were significantly lower in the mice (P<0.05). Compared with the model group, the DAI, CMDI score, unit colon weight, colon tissue MDA content and p62 protein expression were significantly lower in mice in the atractylenolide III group (P<0.05), and the colon length, colon tissue SOD, GSH-PX content and Beclin-1, LC3II/LC3Ⅰ protein expression were significantly higher in mice (P<0.05). The autophagy inhibitor prevented the increase of Beclin-1、LC305). T protein expression induced by Atractylenolide III and inhibited the SOD and GSH-PX contents of colon tissue.Conclusion Atractylenolide III significantly ameliorated the pathological injury of UC and exerted therapeutic effects on UC mice by scavenging peroxides through regulating autophagy levels.objective To investigate whether Atractylenolide III alleviates ulcerative colitis (UC) in mice by scavenging peroxide through regulating autophagy levels.

AR285.5

贵州省科学技术厅科技计划项目基础研究课题（黔科合LH字[2017]7295号）：基于IEC-6细胞探索白术茯苓有效成分治疗克罗恩病机理的实验研究，负责人：任燕；铜仁市科技局支撑计划项目课题研究（铜科成合〔2020〕02号）：道地药材黄精高端产品研发及产业化应用研究，负责人：罗春丽。