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目的观察嗜酸乳杆菌联合美沙拉嗪对小鼠溃疡性结肠炎(UC)的治疗作用,并探讨其可能的作用机制。方法 2.5%DSS 7d建立急性UC动物模型。将70只BALB/c小鼠随机分为7组:分别为正常组、模型组、阴性对照(生理盐水,NS)组、美沙拉嗪组、嗜酸乳杆菌低剂量组(106CFU/ml)、嗜酸乳杆菌高剂量组(108CFU/ml)、嗜酸乳杆菌联合美沙拉嗪组,观察指标包括:疾病活动指数(DAI)、结肠粘膜肉眼改变及病理组织学积分;采用免疫组化SABC法检测热休克蛋白70(HSP70)和c-Jun氨基末端激酶(JNK)的表达量;结果嗜酸乳杆菌可降低实验小鼠DAI积分和改善结肠组织损伤;与模型组、阴性对照组相比,嗜酸乳杆菌低、高剂量组、嗜酸乳杆菌联合美沙拉嗪组JNK蛋白的表达下降(P<0.05),HSP70的表达增加(P<0.05),其中以嗜酸乳杆菌联合美沙拉嗪组效果最佳。结论嗜酸乳杆菌和美沙拉嗪对小鼠溃疡性结肠炎都有治疗作用,且二者疗效相当;两药联合应用效果最佳。其机制可能与抑制JNK的激活、增加结肠粘膜HSP70的表达有关。
Objective To observe the therapeutic effect of Lactobacillus acidophilus and mesalazine on murine ulcerative colitis (UC) and to explore its possible mechanism. Methods 2.5% DSS 7d animal models of acute UC were established. Seventy BALB / c mice were randomly divided into 7 groups: normal group, model group, negative control (NS) group, mesalazine group, low dose group of Lactobacillus acidophilus (106CFU / ml) Lactobacillus acidophilus high dose group (108CFU / ml), Lactobacillus acidophilus combined mesalazine group, the observation indicators include: disease activity index (DAI), colonic mucosal changes and histopathological score; using immunohistochemical SABC method The expression of heat shock protein 70 (HSP70) and c-Jun N-terminal kinase (JNK) was detected. Results Lactobacillus acidophilus could reduce DAI score and improve colonic tissue injury. Compared with model group and negative control group, The expression of JNK protein in Lactobacillus acidophilus low and high dose group and Lactobacillus acidophilus combined with mesalazine group decreased (P <0.05), and the expression of HSP70 increased (P <0.05), and Lactobacillus acidophilus combined with mesalazine Group best. Conclusion Lactobacillus acidophilus and mesalazine have therapeutic effects on mouse ulcerative colitis, and the curative effect is equivalent; the combination of the two drugs has the best effect. The mechanism may be related to the inhibition of JNK activation and the increase of colonic mucosal HSP70 expression.