目的 通过代谢组学方法分析雷公藤甲素（TP）对溃疡性结肠炎（UC）小鼠内源性代谢物的影响，探讨TP干预UC的代谢途径和可能的机制。方法 将C57BL/6小鼠随机分为对照组、模型组、TP组，采用葡聚糖硫酸钠（DSS）诱导UC小鼠模型。采用高效液相色谱-质谱（HPLC-MS）技术检测小鼠血清样本，并结合主成分分析（PCA）和正交偏最小二乘判别分析（OPLS-DA）对各组小鼠血清代谢差异进行表征，筛选出血清中潜在的差异代谢物及可能的代谢通路。结果 与对照组比较，模型组小鼠血清中发现并鉴定出胆酸、牛黄胆酸、鹅去氧胆酸、瓜氨酸、胍基丁酸、氨基乙酸、顺乌头酸等15个差异代谢物。与模型组比较，给予TP干预后，上述潜在差异代谢物有向正常水平回调的趋势。结论 代谢组学分析揭示TP对UC小鼠具有一定的干预作用，其机制可能与调节初级胆汁酸生物合成、精氨酸和脯氨酸代谢等有关。

Objective The effect of triptolide (TP) on endogenous metabolites in mice with ulcerative colitis (UC) was analyzed by means of metabolomics, and the metabolic pathway and possible mechanism of TP in UC were discussed. Methods C57BL/6 mice were randomly divided into blank control group, model group, and triptolide group. Dextran sulfate (DSS) was used to induce UC mice model. The serum samples of mice were detected by high performance liquid chromatography-mass spectrometry and characterized by principal component analysis (PCA) and orthogonal partial least squares discriminant analysis (OPLS-DA) to identify the potential biomarkers and possible metabolic pathways. Results Compared with the blank control group, a total of 15 potential biomarkers, such as cholic acid, bezoar cholic acid, goose-deoxycholic acid, citrulline, guanidine butyric acid, aminoacetic acid, and cis-aconitic acid, were found and identified in serum. Compared with the model group, the potential biomarkers showed a tendency of callback to normal level after TP intervention. Conclusion Metabolomics analysis reveals that TP had certain therapeutic effects on UC mice, and its mechanism may be related to regulating primary bile acid biosynthesis, arginine, and proline metabolism.

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国家自然科学基金资助项目（81760812）；云南省科学技术厅-云南中医药大学应用基础研究联合专项资助[2017FF117(-035)，2018FF001(-021)]