益生菌VSL#3治疗大鼠溃疡性结肠炎的疗效观察及对STAT6、STAT4的影响

目的观察益生菌VSL#3对葡聚糖硫酸钠(dextran sulfate sodium,DSS)诱导大鼠溃疡性结肠炎(ulcerative colitis,UC)的疗效和对信号转导与转录活化因子STAT4、STAT6蛋白表达的影响,了解益生菌VSL#3治疗大鼠实验性结肠炎的可能作用机制。方法采用5%DSS溶液诱导建立UC模型,32只SD大鼠随机分为4组:正常对照组、模型组、美沙拉嗪组、益生菌组,每组8只。模型组、美沙拉嗪组、益生菌组均采用5%DSS溶液造模,正常对照组正常饮食,美沙拉嗪组给予美沙拉嗪混悬液灌胃,益生菌组给予益生菌VSL#3灌胃;采用组织损伤学评分及HE染色检测各组干预疗效,免疫组化及Western blotting法检测大鼠大肠组织中STAT4和STAT6的表达。结果模型组大鼠组织病理损伤最重,明显高于正常对照组、美沙拉嗪组和益生菌组(P0.05)。与模型组比较,美沙拉嗪组和益生菌组大鼠结肠黏膜组织破坏明显减轻,破坏程度介于正常对照组和模型组之间。与模型组比较,益生菌组、美沙拉嗪组STAT4蛋白和STAT6蛋白表达均降低(P0.05)。结论益生菌VSL#3对大鼠UC有治疗作用,其部分机制可能是通过抑制STAT4和STAT6的表达水平而发挥治疗作用。

Effect of probiotic VSL # 3 in treatment of ulcerative colitis in rats and the influence on STAT6, STAT4

Objective To investigate the therapetutic efficacy of VSL#3 against ulcerative colitis （UC） of rats which induced by dextran sulfate sodium （DSS） and its effects on the expression of STAT4 and STAT6 and to learn the possible mechanism of probiotic VSL # 3 treating rats with UC.Methods UC model was induced by 5％ DSS solution,32 male rats were randomly divided into 4 groups：normal control group,model group,mesalazine group and probiotics group.There were eight rats per group.The rats were induced by 5％ DSS in model group,mesalazine group and probiotics group,normal control group was normal diet.The rats in mesalazine group and probiotics group were given mesalazine and VSL#3 through intragastric respectively.The intervention effects were deteeted by hematoxylin-eosinstaining （HE）and tissue damage.The expression of STAT4 and STAT6 of UC tissues were detected by immunohistochemistry and Western blotting.Results Pathological damage in model group was significantly higher than other groups （P ＜ 0.05）.Compared with model group,the damages of tissue in mesalazine group and probiotic group were significantly reduced and between the model group and the normal group.Compared with model group,the expression of STAT4 and STAT6 in probiotic group and mesalazine group were decreased （P ＜ 0.05）.Conclusion Probiotic VSL # 3 has a therapeutic effect on UC in rats,part of the mechanism may be that it plays a therapeutic role through the inhibition of the expression levels of STAT4 and STAT6.