目的 探讨消食白头翁汤对溃疡性结肠炎小鼠的作用及机制。方法 采用随机数表法将小鼠分为正常 组、模型组、美沙拉秦组、消食白头翁汤低剂量组、消食白头翁汤高剂量组，用“高脂高糖饮食+白酒+人工 气候培养箱”造模方式建立 3% 葡聚糖硫酸钠（DSS）诱导的大肠湿热证溃疡性结肠炎小鼠模型，灌胃给予相应 药物及纯水，造模周期共 22 d。计算疾病活动指数和结肠组织病理学评分，测量结肠长度，HE 染色观察结肠 组织形态学变化，ELISA 法检测结肠组织 IL-1β、TNF-α 水平，采用超高效液相色谱串联傅里叶变换质谱联用 仪检测小鼠结肠内容物代谢物水平，确定差异代谢物及相关通路。结果 与正常组比较，模型组小鼠疾病活动 系数（DAI）评分升高（P＜0.001）、结肠组织病理评分升高（P＜0.01）、结肠长度缩短（P＜0.001），IL-1β 和 TNF-α 水平升高（P＜0.01，P＜0.001）；与模型组比较，消食白头翁汤高剂量组小鼠 DAI 评分降低（P＜0.05）、 结肠组织病理评分降低（P＜0.01）、结肠长度更长（P＜0.01），IL-1β 和 TNF-α 水平降低（P＜0.05，P＜0.01）， 且一般症状明显改善。代谢组学表明消食白头翁汤主要影响核苷类代谢物水平及嘧啶代谢、甘油磷脂代谢、酪 氨酸代谢及初级胆汁酸代谢通路。结论 消食白头翁汤对溃疡性结肠炎具有治疗作用，其机制可能与调节菌群 核苷类物质代谢及影响嘧啶代谢通路有关。

Objective To investigate the therapeutic effects and underlying mechanisms of Xiaoshi Baitouweng Decoction （XBD） in ulcerative colitis （UC） mice. Methods Mice were randomized into normal，model，Mesalazine， XBD low-dose， and XBD high-dose groups using a random number table. A UC mouse model with "damp-heat syndrome of the large intestine" was established via a "high-fat high-sugar diet + alcohol + artificial climate incubator" protocol combined with 3% dextran sodium sulfate （DSS）. Corresponding treatments or pure water were administered via gavage over a 22-day modeling period. Disease activity index （DAI） and histopathological scores were calculated， colon length was measured，and colon morphology was assessed via hematoxylin-eosin （HE） staining. ELISA was used to detect IL-1β and TNF-α levels in colon tissues，while ultra-high-performance liquid chromatography coupled with Fourier transform mass spectrometry （UHPLC-FTMS） analyzed colonic metabolite profiles to identify differential metabolites and associated pathways. Results Compared with the normal group，the model group exhibited elevated DAI scores （P＜0.001） and histopathological scores （P＜0.01），shortened colon length （P＜0.001），and increased IL-1β and TNF-α levels （P＜0.01 and P＜0.001）. Compared with the model group，the XBD high-dose group showed reduced DAI scores （P＜0.05） and histopathological scores （P＜0.01），longer colon length （P＜0.01），decreased IL-1β and TNF- α levels （P＜0.05 and P＜0.01）， and significant alleviation of clinical symptoms. Metabolomics revealed that XBD primarily modulated nucleoside-related metabolites and pathways including pyrimidine metabolism， glycerophospholipid metabolism， tyrosine metabolism， and primary bile acid biosynthesis. Conclusion XBD exerts therapeutic effects on UC， potentially mediated by regulating microbial nucleoside metabolism and influencing pyrimidine metabolic pathways.

R285.5

广东省基础与应用基础研究基金项目（2022A1515140124 ，2023A1515140115）。