健脾清肠方联合骨化三醇对溃疡性结肠炎大鼠白细胞介素-17和干扰素-γ表达的影响

Effects of Jianpi Qingchang Decoction Combined with Calcitriol on IL-17 and IFN-γin Ulcerative Colitis Rats

目的观察健脾清肠方联合骨化三醇对溃疡性结肠炎大鼠结肠黏膜白细胞介素-17(IL-17)和干扰素-γ(IFN-γ)表达的影响,探讨其作用机制。方法实验大鼠随机分为正常组、模型组、美沙拉嗪组、骨化三醇组、健脾清肠方+骨化三醇组,每组10只。除正常组外,其余各组大鼠予三硝基苯磺酸灌肠造模。造模后第3日大鼠开始给药,开始给药后第11日称重后处死。期间计算疾病活动指数(DAI),光镜下按结肠组织病理学评分(HPS)评估大鼠结肠黏膜损伤程度。采用RT-PCR和免疫组化方法检测结肠黏膜IFN-γ、IL-17 m RNA和蛋白表达。结果模型组DAI及HPS明显高于正常组(P<0.01);与模型组比较,各给药组DAI及HPS显著降低(P<0.05,P<0.01),美沙拉嗪组和健脾清肠方+骨化三醇组大鼠结肠黏膜IFN-γ、IL-17 m RNA和蛋白表达明显降低(P<0.01)。结论健脾清肠方联合骨化三醇可能通过调节大鼠辅助T淋巴细胞17细胞,下调IL-17表达,降低免疫细胞活性,减少炎性细胞分泌,减轻结肠黏膜的损伤。

Objective To investigate the effects of Jianpi Qingchang Decoction combined with Calcitriol on the expressions of IL-17 and IFN-γin colitis in rats with ulcerative colitis;To discuss the mechanism of action.Methods Experimental rats were randomly divided into control group,model group,Mesalazine group,Calcitriol group,Jianpi Qingchang Decoction+Calcitriol group,with 10 rats in each group.Except for the control group,other groups were given TNBs for modeling.The administration began on the 3rd day after modeling.All rats were weighed and sacrificed on the 11th day after administration.The disease activity index(DAI)were calculated and the colon histopathological(HPS)were evaluated under microscope.The mRNA and protein expressions of IFN-γand IL-17 in colonic mucosa were detected by RT-PCR and immunohistochemistry.Results Compared with the control group,the DAI and HPS of the model group increased significantly(P<0.01);Compared with the model group,the DAI and HPS of administration groups were reduced significantly(P<0.05,P<0.01),and the mRNA and protein expressions of IFN-γand IL-17 in Mesalazine group and Jianpi Qingchang Decoction+Calcitriol group decreased significantly(P<0.01).Conclusion Jianpi Qingchang Decoction combined with Calcitriol can down-regulate IL-17 expression,decrease the activity of immune cells,reduce the secretion of inflammatory cells,and lessen the damage of colonic mucosa by regulating Th17 cells.