缺血后处理对大鼠肠缺血-再灌注损伤肠黏膜细胞线粒体的影响

Effects of ischemic postconditioning on intestinal mucosa mitochondrion after ischemia-reperfusion injury in rat intestine

目的探讨缺血后处理对大鼠肠缺血-再灌注损伤肠黏膜细胞线粒体的影响。方法SD大鼠32只随机分为4组(n=8):假手术(S)组、缺血-再灌注(I/R)组、缺血预处理(IPC)组、缺血后处理(I-post)组。应用透射电子显微镜、四甲基偶氮唑蓝(MTT)比色法、激光共聚焦扫描显微镜分别观测各组大鼠肠黏膜细胞线粒体的形态结构、呼吸功能以及线粒体跨膜电位的变化。结果与I/R组相比,I-post组和IPC组大鼠肠黏膜细胞线粒体形态结构改变明显减轻,线粒体呼吸功能和线粒体跨膜电位明显升高(P<0.05);I-post组与IPC组相比,差异无统计学意义(P>0.05)。结论缺血后处理抗大鼠肠缺血-再灌注损伤的作用机制可能与改善肠黏膜细胞线粒体的形态结构和呼吸功能及提高线粒体跨膜电位有关。

Objective To investigate the effects of ischemic postconditioning （Ⅰ-post） on intestinal mucosa mitochondrion after ischemia-reperfusion （I/R） injury in rat intestine. Methods By using rat model of intestine I/R injury, male Sprague-Dawley rats were divided into 4 groups： sham-operation group （S）, I/R group （I/R）, ischemic preconditioning group （IPC）, and Ⅰ-post group. Intestinal mucosa mitochondrial ultrastructural changes were observed by using transmission electron microscope （TEM）. Mucosal cellular mitochondrial respiration function was studied by measuring the mitochondrial dehydrogenase-dependent reduction of MTT to its formazan derivative, and intestinal mucosal mitochondrial membrane potential was detected by confocal laser scanning microscopy. Results Compared with that in I/R group, the injury of mitochondrion in Ⅰ-post group and IPC group began to recover. The mitochondrial respiratory function and the mitochondrial membrane potential were significantly improved in Ⅰ-post group and IPC group （P〈0.05）. There were no significant differences between Ⅰ-post group and IPC group （P〉0.05）. Conclusion The mechanism of ischemic postconditioning against I/R injury of intestine in rats is partly related to maintaining the mitochondrial ultrastructural changes and respiratory function and improving mitochondrial membrane potential.