缺血后适应对大鼠局灶性脑缺血再灌注后细胞凋亡的影响

目的：探讨缺血后适应对大鼠局灶性脑缺血再灌注损伤后细胞凋亡的影响。方法：大脑中动脉线拴法复制大鼠局灶性脑缺血再灌注损伤动物模型。将30只雄性SD大鼠随机分为假手术（sham）组、脑缺血再灌注（I／R）组和缺血后适应（IP）组，每组10只。利用原位缺口末端标记法研究神经细胞凋亡的变化。应用Westernblotting检测大鼠局灶性脑缺血再灌注损伤后P38和Caspase一3蛋白表达水平的变化。结果：大鼠脑缺血再灌注后凋亡细胞数量，P38和Caspase-3蛋白表达水平均显著升高，而缺血后适应组凋亡细胞数量，P38和Caspase-3蛋白表达水平均显著低于缺血再灌注组（P〈0．01）。结论：缺血后适应可减少大鼠脑缺血再灌注后细胞凋亡的发生，此作用可能与抑制P38和Caspase-3蛋白表达有关。

Effect of ischemic postconditioning on apoptosis after focal cerebral ischemia reperfusion in rat

Objective： To investigate the effect of ischemic postconditioning on apoptosis after focal cerebral ischemia reperfusion in rat. Methods：A rat model of focal cerebral ischemia-reperfusion injury was established by middle cerebral artery occlusion using modified filament method. Male Sprague-Dawley rats were randomized into 3 groups （n=10）： sham-operate（sham） group, isehemia/reperfusion（I/R） group and ischemic postconditioning （IP） group. TUNEL assay was employed to examine the cell apoptosis and Western blotting analysis were used to detect the expression of P38 and Caspase-3 proteins. Results：The apoptotic cells and protein expression of P38 and Caspase-3 increased markedly after cerebral ischemiareperfusion injury in rats. While the apoptotic cells and protein expression of P38 and Caspase-3 decreased significantly in the IP group compared with the I/R group （P〈0.01）. Conclusion： Ischemic postconditioning decrease the protein expression of P38 and Caspase-3 after focal cerebral ischemia reperfusion in rat, which might be an important mechanism of apoptosis.