IL-33在小鼠炎症性肠病中的保护作用研究

Effect of IL-33 on inflammatory bowel disease in mice

目的探讨白介素(IL)-33在小鼠炎症性肠病中的保护作用。方法建立TNBS诱导的小鼠炎症性肠病模型,设立乙醇空白对照组、模型组和IL-33治疗组。HE染色观察结肠组织病理形态学变化;免疫荧光检测组织M2型巨噬细胞数量变化;RT-PCR检测结肠组织i NOS、YM1和Arg1基因表达。结果模型组小鼠结肠组织病理损伤严重,而IL-33处理后能明显缓解结肠炎症损伤程度。IL-33上调M2型巨噬细胞数量及M2型相关基因YM1、Arg1表达。结论 IL-33能缓解TNBS诱导的小鼠结肠炎,可能与促进M2型巨噬细胞极化相关。

Objective To investigate the effect of interleukin-33 （IL-33） on TNBS-induced inflammatory bowel disease in mice. Methods The inflammatory colitis model was established by colonic delivery of TNBS in mice. The mice were divided into three groups, including the ethanol control group, the TNBS group and IL-33-treated group. The changes of colonic histological morphology were observed by H＆E staining. The number of M2-type macrophages was measured by immunofluorescence. The gene expression of iNOS, YM1 and Arginase-1 was detected by RT-PCR. Results Compared with the control group, treatment with IL-33 reduced the pathological damage of colon in mice. The number of M2-type macrophages and the expression of M2-type associated gene YM1 and Arginase-1 were increased in IL-33-treated mice. Conclusion IL-33 plays a protection against TNBS-induced colitis in mice, possibly through promoting the polarization of M2-type macrophages.