缺血后处理对缺血-再灌注大鼠肠黏膜的抗损伤作用

The role of ischemic postconditioning on intestinal mucosa in rats with ischemia-reperfusion injury

目的探讨缺血后处理对缺血-再灌注大鼠肠黏膜的抗损伤作用。方法复制SD大鼠肠缺血-再灌注损伤模型。实验分为4组(n=8):假手术组(S)、缺血-再灌注组(I/R)、缺血预处理组(IPC)、缺血后处理组(I-post)。比较各组大鼠肠黏膜丙二醛(MDA)含量、超氧化物歧化酶(SOD)和髓过氧化物酶(MPO)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)检测肠黏膜细胞凋亡发生率;Chius评分法观察肠黏膜的损伤情况。结果与I/R组相比,IPC组和I-post组大鼠肠黏膜MDA含量和MPO活性均显著降低,而SOD活性明显升高;再灌注后可见明显的肠黏膜细胞凋亡现象,I-post组和IPC组凋亡指数较I/R组显著下降,组织病理损伤亦明显减轻。I-post组和IPC组相比,各项指标无显著性差异。结论缺血后处理可通过抑制再灌注后氧自由基的过量产生,保护抗氧化系统,从而抑制肠黏膜细胞凋亡,减轻肠缺血-再灌注损伤。

Objective To investigate the role of ischemic postconditioning （I-post） on intestinal mucosa in rats with ischemia-reperfusion （I/R） injury. Methods By using rat model of intestine I/R injury, 32 male Sprague- Dawley rats were randomly divided into 4 groups： sham-operation group （S）, I/R group （I/R）, ischemic preconditioning group （IPC）, and ischemic postconditioning group （I-post）, respectively. The contents of malondialdehyde （MDA）, the activity of superoxidase dismutase （SOD）, and the activity of myeloperoxidase （MPO） in intestinal mucosa were measured respectively. The status of intestinal mucosa cellular apoptosis was detected by TdT-mediated dUTP-biotin nick end labeling （TUNEL）. Chiu＇s count was used to assess the changes in intestinal pathological morphology. Results The content of MDA and activity of MPO were significantly reduced and the activity of SOD was enhanced in IPC group and I-post group compared with I/R group. There was obvious cellular apoptosis after reperfusion, and the apoptotic index in I-post group and IPC group was significantly lower than that in I/R group. Conclusion Ischemic postconditioning can result in protection against intestinal mucosa with I/R injury, which may be related to reducing the production of oxygen free radicals, maintaining the activities of antioxidant systems, and reducing intestinal mucosa cellular apoptosis.