益生菌对阿司匹林致大鼠急性胃黏膜损伤的作用机制  

Protective effect of probiotics on aspirin-induced gastric mucosal lesions in rats

作　　者：高欣[1] 张振玉[1] 吴海露[1] 陈菲菲[1] 杨小兵[2] 王劲松[2] 

机构地区：[1]南京医科大学附属南京医院消化科,江苏省南京市210006 [2]南京医科大学附属南京医院病理科,江苏省南京市210006

出　　处：《世界华人消化杂志》2012年第30期2882-2887,共6页World Chinese Journal of Digestology

摘　　要：目的:研究益生菌对阿司匹林引起的大鼠急性胃黏膜损伤的影响及其机制.方法:40只健康♂SD大鼠随机分为4组,每组10只:对照组、损伤组、培菲康组和亿活组.培菲康和亿活组的大鼠分别用相应益生菌制剂灌胃进行预处理,然后将除对照组以外所有大鼠以150mg/kg阿司匹林灌胃造成急性胃黏膜损伤;分别测定各组大鼠的胃黏膜损伤指数(lesionindex,LI);观察大鼠胃黏膜组织学变化;免疫组织化学法检测各组胃黏膜上皮紧密连接蛋白Occludin的表达情况;免疫蛋白印迹法(Western blot)检测紧密连接蛋白Occludin和MAPK信号通路中磷酸化p38蛋白的表达量.结果:与损伤组相比,两组益生菌组(培菲康组和亿活组)胃黏膜损伤较损伤组均减轻(18.4±3.69、17.1±3.84vs25.8±4.94,P<0.05);大鼠胃黏膜中的紧密连接蛋白Occludin在损伤组的表达与对照组相比下降(P<0.05),而在两组益生菌组中的表达则较损伤组增加(P<0.05)大鼠胃黏膜中磷酸化p38蛋白在损伤组的表达与对照组相比增加(P<0.05),而在两组益生菌组中的表达则较损伤组下降(P<0.05).结论:益生菌制剂培菲康和亿活对阿司匹林引起的大鼠急性胃黏膜损伤均具有明显保护作用,其机制可能与通过MAPK中的p38信号通路上调胃黏膜上皮黏膜紧密连接蛋白Occludin的表达进而增强了大鼠胃黏膜的物理屏障功能有关.AIM： To determine the protective effect of probiotics on aspirin-induced gastric mucosal lesions in rats.METHODS： Forty healthy male SD rats were randomly and equally divided into four groups： normal group, injury group, and two probiotics groups （bifico group and bioflor group）. Gastric mucosal lesions were induced by gastric gavage of aspirin （150 mg/kg）. Rats of probiotics groups were pretreated with probiotics before induction of gastric mucosal lesions. Gastric histological changes were evaluated under a microscope. Immunohistochemistrv and Western blot wereused to detect the distribution and expression of gastric epithelial tight junction protein occludin. The expression of phosphorylated-p38 （p-p38） was determined by Western blot.RESULTS： Compared to the injury group, lesion indices were significantly decreased in the probiotics groups （18.4 ± 3.69, 17.1 ±3.84 vs 25.8 ± 4.94, both P 〈 0.05）. The expression level of occludin in the injury group was decreased sig- nificantly compared to the normal group （P 〈 0.05）. However, the expression levels of occludin in the two probiotics groups were significantly higher than that in the injury group （both P 〈 0.05）. Phosphorylation of p38 was more obvious in the injury group than in the normal group （P 〈 0.05）. Pretreatment with probiotics significant- ly inhibited the phosphorylation of p38 （P 〈 0.05）.CONCLUSION： Probiotics have a protective ef- fect on aspirin-induced gastric mucosal lesions in rats probably by increasing the expression of tight junction protein occludin via the p38 signaling pathway.

关 键 词：益生菌 阿司匹林 胃黏膜损伤 OCCLUDIN 蛋白 MAPK信号通路 

分 类 号：R573[医药卫生—消化系统]