目的 探究广藿香水提物（PWE）对溃疡性结肠炎（UC）小鼠的治疗作用及潜在机制。方法 将50只小鼠随机分为对照组、模型组、美沙拉嗪（阳性药，0.31 g·kg-1）组及PWE低、高剂量（0.62、2.05 g·kg-1）组。采用2.5%葡聚糖硫酸钠（DSS）自由饮水法诱导小鼠UC模型，造模期间同步ig给药；实验过程中记录小鼠体质量变化，评估疾病活动指数（DAI）。采用酶联免疫吸附法（ELISA）检测结肠组织白细胞介素（IL）-6、肿瘤坏死因子α(TNF-α)、IL-1β、IL-18水平；TUNEL染色检测结肠组织细胞损伤情况；Western blotting与免疫组织化学法检测结肠组织Toll样受体2(TLR2)/核转录因子-κB (NF-κB)/NOD样受体热蛋白结构域相关蛋白3(NLRP3)通路及细胞焦亡相关蛋白[TLR2、髓样分化因子88(My D88)、p-NF-κB、NLRP3、凋亡相关斑点样蛋白（ASC）、Caspase-1、GSDMD）]的表达水平。结果 与模型组相比，PWE高剂量组小鼠体质量显著回升（P<0.01），结肠长度显著延长（P<0.01）,DAI评分、结肠炎症因子（IL-6、TNF-α、IL-1β、IL-18）水平、结肠组织细胞TUNEL染色阳性率显著降低（P<0.01）；同时，结肠组织TLR2、My D88、p-NF-κB、NLRP3、ASC、Caspase-1及GSDMD蛋白表达水平及免疫组化染色强度均显著下调（P<0.01）。结论 PWE对DSS诱导的UC小鼠具有明确治疗效果，其机制可能与调控TLR2/NF-κB/NLRP3通路、抑制结肠细胞焦亡有关。

Objective To investigate the therapeutic effect and potential mechanism of Pogostemon cablin water extract（PWE） in mice with ulcerative colitis（UC）. Methods Fifty mice were randomly divided into the following groups: Control, model, mesalazine(positive drug, 0.31 g·kg^-1), low and high dose of PWE(0.6, 2.05 g·kg^-1) groups. A UC model was induced in mice by freely drinking 2.5% dextran sodium sulfate（DSS）, with simultaneous oral administration of treatments. Changes in body mass were recorded and the disease activity index（DAI） was assessed throughout the experiment. The levels of IL-6, TNF-α, IL-1β and IL-18 in mouse colon tissues were measured by ELISA. TUNEL staining was used to detect the damage of colon cells. Expression of proteins related to TLR2/NF-κB/NLRP3 pathway and pyroptosis in colon tissues [TLR2, myeloid differentiation factor 88（MyD88）, p-NF-κB, NLRP3, apoptosis-associated speck-like protein（ASC）, Caspase-1, GSDMD] was analyzed by Western blotting and immunohistochemistry. Results Compared with the model group, mice intervened with high dose of PWE showed a significant increase in body mass and colon length（P ＜ 0.01）, and significantly reduced levels of DAI scores, colonic inflammatory factors（IL-6, TNF-α, IL-1β and IL-18）, as well as TUNEL positive rates of cells in mouse colon tissue（P ＜ 0.01）. Furthermore, the expression and immunostaining intensities of TLR2, MyD88, p-NF-κB, NLRP3, ASC, Caspase-1 and GSDMD in colonic tissues were significantly downregulated（P ＜ 0.01）. Conclusion PWE exerts a definite therapeutic effect on DSS-induced UC in mice, potentially through regulation of the TLR2/NF-κB/NLRP3 pathway and inhibition of pyroptosis process.

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