缺血后处理对再灌注大鼠胃黏膜细胞的保护作用

The protective role of ischemic postconditioning on ischemia-reperfusion induced gastric mucosa injury in rats

目的探讨缺血后处理对再灌注大鼠胃黏膜的保护作用及其抗氧化机制。方法制备胃缺血后处理模型;实验分为5组(n=6):假手术组(S)、单纯缺血-再灌注组(I-R)、缺血预处理组(IPC)、缺血后处理组(I-post)、缺血后处理+缺血预处理组(I-post+IPC)。记录各组胃黏膜损伤指数并检测胃黏膜丙二醛(MDA)含量、超氧化物歧化酶(SOD)的活性变化;末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法(TUNEL)检测胃黏膜细胞的凋亡。结果与S组相比,I-R组胃黏膜损伤指数和黏膜细胞凋亡率显著升高,胃黏膜MDA含量显著增加,SOD活性明显降低;在IPC组、I-post组和I-post+IPC组,胃黏膜损伤指数与细胞凋亡率较I-R组显著降低,胃黏膜MDA含量也显著降低,而SOD活性明显升高;I-post+IPC组对再灌注的胃黏膜损伤无叠加保护作用,分别与IPC组和I-post组相比,各项指标的差异无统计学意义。结论缺血后处理可显著减轻胃黏膜再灌注损伤,其效应与缺血预处理相似,其机制之一可能与其再灌注后氧自由基的生成减少,抑制胃黏膜细胞膜脂质过氧化、使再灌注的胃黏膜细胞凋亡减轻有关。

Objective To investigate the protective effect of ischemic postconditioning （I-post） on ischemia-reperfusion （I-R） induced gastric mucosa injury in rats. Methods By using rat model of gastric I-R injury, 30 Sprague-Dawley rats were randomly divided into 5 groups： sham operation group （S） , I-R group （I-R） , ischemic preconditioning group （IPC）, ischemic postconditioning group （I-post） and I-post ＋ IPC. Gastric mucosal injury index was recorded. The contents of malondialdehyde （MDA） and the activity of superoxidase dismutase （SOD） of gastric mucosa were measured respectively. The status of gastric mucosa cellula apoptosis was detected by TdT-mediated dUTP-biotin nick end labeling （TUNEL）. Results Ischemia followed by reperfusion leaded to gastric mucosal injury and high gastric mucosal apoptosis rate. The severity of I-R-induced gastric lesions were reduced by IPC, I-post and I-post ＋ IPC. The content of MDA was significantly reduced and the activity of SOD was enhanced in IPC, I-post and I-post ＋ IPC group compared with I-R group. While among IPC, 1-post and I-post ＋ IPC had nosignificant difference. I-post ＋ IPC had no more protective effect on I-R induced gastric mucosal injury. Conclusion I-post can decrease I-R induced gastric mucosa injury. The protective role may be mediate by the same path of IPC which reducing the production of oxygen free radicals and gastric mucosa cellular apoptosis.