参苓白术散治疗炎症性肠病与肠上皮细胞紧密连接的关系探讨

目的:探讨参苓白术散通过肠上皮细胞紧密连接对抗5%葡聚糖硫酸钠(DSS)诱导的小鼠肠炎(IBD)的作用机制。方法:48只SPF级BALB/c小鼠随机分为正常组、模型组、柳氮磺胺吡啶组、参苓白术散低、中、高剂量组,除正常组之外,5%DSS自由饮用7 d诱导BALB/c小鼠急性炎症性肠病,参苓白术散高、中、低剂量组ig分别给予12,6,3 g·kg-1参苓白术散,正常组和模型组ig等体积生理盐水,柳氮磺胺吡啶组ig给予柳氮磺胺吡啶2 g·kg-1,15 d后观察小鼠体重、粪便性状、隐血便血,计算疾病活动度(DAI)积分、病理检测肠黏膜病变。采用Western blot和RT-PCR检测闭合蛋白(Claudin)水平变化和咬合蛋白(Occluding),Claudin,胞浆附着蛋白(ZO-1)和细胞间连接黏附分子(JAM)mRNA表达。结果:与正常组相比,模型组Clandin蛋白表达明显降低(P0.05),Occluding,Claudin,ZO-1和JAM mRNA水平降低(P0.05);给药后,与模型组相比,柳氮磺胺吡啶组、参苓白术散低、中、高剂量组Clandin蛋白表达量明显升高(P0.05),各给药组的Occluding,Claudin,ZO-1和JAM mRNA表达明显升高(P0.05)。结论:参苓白术散抗DSS诱导的IBD的作用与调节肠上皮细胞间细胞紧密连接有关。

Effect of Shenling Baizhu San on Regulation of Tight Junction in DSS-induced IBD Mice

Objective: To investigate the mechanism of Shenling Baizhu San (SLBZS) in treating dextra sulfate sodium (DSS) -induced inflammatory bowel disease (IBD) mice. Method: Eighty SPF BALB/c mice were randomly divided into control group, model group, positive group, low-, medium- and high-dose SLBZS groups. The IBD mice were fed 5% DSS in their drinking water for 7 days, and control mice received only water. The mice in SLBZS groups were given SLBZS at doses of 3, 6, 12 g·kg^-1, the mice in positive group were given mesalazine sustained release granules at dose of 2 g·kg^-1, and the control mice were given the same volume of normal saline by intragastric administration. The mice weight, stool occult blood in the stool, the calculation of disease activity (DAI), pathological examination of intestinal mucosal lesions integral were observed after 15 days. The expression of Claudin protein was tested by Westorn bolt. The expression of Occluding, Claudin, ZO-1 and JAM mRNA were analyzed by RT-PCR. Result: The lesion was obvious, Clandin protein decreased obviously in the model group as compared with the control group (P<0.05). Claudin protein, Occluding, Claudin, ZO-1 and JAM mRNA increased in DSS and all doses SLBZS groups as compared with the control group (P<0.05). Conclusion: SLBZS has good effect in DSS-induced IBD mice by the regulation of intestinal epithelial cell tight junctions.