微生态制剂对TNBS诱导的大鼠结肠炎的疗效

目的:评价双歧三联活菌对三硝基苯磺酸钠(TNBS)诱导的大鼠结肠炎的疗效,并探讨其作用机制.方法:成年♀SD大鼠(n=50),随机分为健康对照组A、未治疗组B、双歧三联活菌治疗组C、奥沙拉秦治疗组D、双歧三联活菌和奥沙拉秦联合治疗组E(n=10).观察大鼠的一般情况,检测各组大鼠血清肿瘤坏死因子-α(TNF-α)、结肠组织TNF-α细胞阳性率,比较结肠组织炎症程度.结果:A组大鼠DAI(P<0.001)、血清TNF-α(P<0.001)水平、肠组织TNF-α细胞阳性率(P<0.05)、肠组织学评分(P<0.05)显著低于未治疗组B;B组大鼠DAI、血清TNF-α水平、肠组织学评分、肠组织TNF-α细胞阳性率最高(P<0.05);3个治疗组C、D、E的大鼠DAI、血清TNF-α、肠组织TNF-α细胞阳性率明显下降,肠组织炎症明显消散,以E组最显著(P<0.05),肠组织TNF-α的表达与结肠炎病情轻重呈正相关.结论:双歧三联活菌能有效治疗TNBS诱导的大鼠结肠炎,其作用机制可能与抑制肠黏膜免疫系统效应细胞TNF-α的表达有关.

Therapeutic effect of a probiotic compound on TNBSinduced colitis in rats

AIM:To evaluate the therapeutic effect of a probiotic compound on colitis in rats induced with trinitrobenzenesulfonic acid(TNBS)and to investigate the underlying mechanisms.METHODS:In total,50 female adult SpragueDawley rats were randomized into five groups:healthy control group(A),untreated group(B),probiotics group(C),olsalazine group(D)and combined treatment group(E).Except for groupA,rats in the other groups were subjected to induction of colitis.Each group received a corresponding therapeutic regimen.After treatment,the general status of all rats was observed;serum levels of tumor necrosis factor-alpha(TNF-α) and positive rate of colonic TNF-αexpression in the colon were detected;and histopathologic changes in the colon were examined.RESULTS:The disease activity index(DAI),serum levels of TNF-α,positive rate of TNF-α expression in the colon,and histopathologic score were significantly lower in group A than in group B(all P<0.05).Group B exhibited most severe colonic inflammation and highest DAI,serum TNF-α,and positive rate of TNF-α expression in the colon(all P<0.05).The three treatment groups(C,D and E)showed marked remission of colonic inflammation and significantly decreased serum TNF-αand positive rate of TNF-αin the colon when compared to group B(all P<0.05),with group E being most prominent.Colonic TNF-αexpression correlates positively with the severity of colitis.CONCLUSION:The tested probiotic compound could effectively reduce TNBS-induced colitis in rats possibly via mechanisms associated with the inhibition of TNF-αexpressed by the effector cells of intestinal mucosal immune system.