固肠胶囊对慢性溃疡性结肠炎大鼠炎症介质及结肠黏膜的影响

Effects of Guchang capsules on expression of inflammatory mediators and colonic mucosa in ulcerative colitis rats

关键词:  慢性溃疡性结肠炎  固肠胶囊  肿瘤坏死因子-α  白细胞介素-10

Key words:  chronic ulcerative colitis  Guchang capsules  TNF-α  IL-10

摘要:

[目的]观察固肠胶囊对慢性溃疡性结肠炎(UC)大鼠血清肿瘤坏死因子-α(TNF-α)和白细胞介素-10(IL-10)水平及结肠病理组织的影响,探讨其可能作用机制.[方法]Wistar大鼠随机分为空白对照组、模型组、固肠胶囊高、中、低剂量组,采用三硝基苯磺酸(TNBS)/乙醇溶液及葡聚糖硫酸钠(DSS)联合应用复制大鼠慢性UC模型,于造模缓解复发期灌胃给药10 d,观察各组大鼠疾病活动指数(DAI),结肠黏膜损伤指数(CMDI)及病理组织学改变,酶联免疫吸附法(ELISA)测定血清TNF-α、IL-10水平.[结果]与空白对照组比较,模型组DAI、 CMDI评分及血清TNF-α水平显着升高(P<0.01),IL-10水平显着降低(P<0.01).与模型组比较,固肠胶囊能明显升高血清IL-10水平(P<0.05),降低DAI、CMDI评分(P<0.01)及血清TNF-α水平(P<0.05),促进溃疡修复.[结论]固肠胶囊可通过抑制血清TNF-α表达、促进血清IL-10表达,抑制炎症进展,减轻结肠组织因过度免疫介导作用而导致的肠黏膜损伤而治疗慢性UC.

Abstract:

[Objective] To observe the effects of Guchang capsules on expression of expression of inflammatory mediators and intestinal mucosa in chronic ulcerative colitis (UC) rats, and explore its mechanism. [Methods] Wistar rats was randomly divided normal group, model group, Guchang cupsules high dose, middle dose and low dose group,2,4,6 trinitrobenzene sulfonic acid(TNBS)/ethanol solution and dextran sulfate sodium(DSS)was administrated to make chronic ulcerative colitis rats models. Rats were treatmented for 10 days, then, ats' disease activity index(DAI), colonic mucosal damage index(CMDI) and the histological changes were assessed. Enzyme-linked immunosorbent assay (ELISA) methods was used to determine the expression of TNF-α and IL-10 in blood serum. [Results] Compared with normal group, DAI and CMDI sores, and TNF-α content of model group were significantly increased(P<0.01). IL-10 contentas significantly decreased(P<0.01). Compared with model group, Guchang capsules could significantly increase IL-10 content(P<0.05), decrease DAI scores, CMDI sores(P<0.01) and TNF-α content(P<0.05), and promote the restoration of the facilitate ulcer. [Conclusion] By increasing IL-10 expression and decreasing TNF-α expression, Guchang capsules can limit inflammation progress and ruduce colonic mucosal damage induced by exceesive immune mediated role to treat UC consequently.