缺血后处理对再灌注损伤大鼠胃黏膜细胞ERK表达的影响  

Effects of ischemic post-conditioning on extracellular signal-regulated kinase expression in the gastric mucosa in rats with GI-R injury

作　　者：丁雷[1] 杜东书[2] 张建福[2,3] 

机构地区：[1]徐州医学院病理生理学教研室,江苏徐州221002 [2]徐州医学院神经生物学研究中心 [3]徐州医学院生理学教研室

出　　处：《徐州医学院学报》2009年第12期787-790,共4页Acta Academiae Medicinae Xuzhou

基　　金：国家自然科学基金(30570671);徐州医学院科研课题(08KJ11)

摘　　要：目的探讨缺血后处理(ischemic post-conditioning,I-postC)对大鼠胃黏膜再灌注(GI-R)损伤的影响及细胞机制。方法制备胃缺血后处理模型。实验分为3组(n=6):假手术组(Sham组)、缺血-再灌注组(I-R组)、缺血后处理组(I-postC组)。用末端脱氧核苷酸转移酶介导的d UTP缺口末端标记法(TUNEL)检测胃黏膜细胞的凋亡,用免疫组化方法检测胃黏膜细胞增殖及凋亡相关基因p-ERK的表达。结果与Sham组相比,I-R组胃黏膜细胞凋亡增加及增殖减少,p-ERK表达下调;与I-R组相比,缺血后处理显著降低胃黏膜细胞凋亡率,同时可以增加胃黏膜增殖率及p-ERK的表达。结论缺血后处理可抑制胃黏膜细胞凋亡,促进细胞增殖。其机制可能与p-ERK的表达上调有关。Objective To investigate the effects and cellular mechanism of ischemic post-conditioning（I-postC） on I/R-induced gastric mucosal injury in rats.Methods Animal model of gastric I-R injury was established in 18 Sprague-Dawley rats,which were randomly divided into 3 groups： sham group,I-R group and ischemic post-conditioning group（I-postC group）.TdT-mediated dUTP-biotin nick end labeling（TUNEL） was employed to detect the gastric mucosal cells apoptosis,and employed to detect the immunohistochemistry employed to detect the expression of p-ERK.Results Compared with Sham group,the gastric mucosal cellular apoptosis in I-R group increased,the proliferation decreased,and the expression of p-ERK was down-regulated.Compared with I-R group,ischemic post-conditioning could markedly reduce gastric mucosal cellular apoptosis,and meanwhile increase the proliferation rate of gastric mucosa and promote the protein expression of p-ERK.Conclusion The I-postC inhibites cellular apoptosis and promotes cellular proliferation and its protective mechanism is associated with the up-regulated expression of p-ERK.

关 键 词：胃缺血-再灌注 缺血后处理 细胞外信号调节激酶 

分 类 号：R364[医药卫生—病理学]