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目的探讨参青方治疗溃疡性结肠炎的作用机制。方法采用三硝基苯磺酸灌肠诱导建立大鼠溃疡性结肠炎模型。SD大鼠60只,随机分为正常组、模型Ⅰ组、模型Ⅱ组、美沙拉嗪组、参青方低剂量组、参青方高剂量组共6组,每组10只。运用免疫组织化学染色、RT-PCR、Western-blot实验技术检测模型大鼠结肠黏膜地址素细胞黏附分子(MAdCAM-1)的表达。结果正常组大鼠结肠黏膜MAdCAM-1可见少量表达,模型组MAdCAM-1蛋白表达与基因转录量均高于正常组,差异具有统计学意义(P<0.01);参青方高、低剂量组及美沙拉嗪组与模型Ⅱ组比较,MAdCAM-1的表达均明显下调,差异具有统计学意义(P<0.01),且以参青方高剂量组降低趋势更为明显。结论参青方具有治疗大鼠溃疡性结肠炎的作用,其机制与降低MAdCAM-1在结肠黏膜的表达有关。
Objective To explore the mechanism of Shen Qing Fang in the treatment of ulcerative colitis. Methods The rat model of ulcerative colitis was induced by trinitrobenzene sulfonic acid enema. Sixty SD rats were randomly divided into normal group, model group Ⅰ, model Ⅱ group, mesalazine group, ShenQingFang low dose group and ShenQingFang high dose group, with 6 in each group. Immunohistochemical staining, RT-PCR and Western-blot were used to detect the expression of MAdCAM-1 in colonic mucosa. Results The expression of MAdCAM-1 in the normal mucosa of rats in normal group was lower than that in normal group (P <0.01). The expression of MAdCAM-1 protein and gene in model group were higher than those in normal group And the mesalazine group compared with the model group, the expression of MAdCAM-1 was significantly down-regulated (P <0.01), and the decreasing trend was more obvious in the high-dose ShenQingFang group. Conclusions ShenQingFang can treat ulcerative colitis in rats, the mechanism of which is related to decreasing the expression of MAdCAM-1 in colonic mucosa.