后适应对大鼠脑缺血神经细胞凋亡和内皮型一氧化氮合酶与诱导型一氧化氮合酶的影响

目的：研究缺血耐受（后适应和预适应）对脑缺血再灌注神经细胞凋亡及内皮型一氧化氮合酶（eNOS）和诱导型一氧化氮合酶（iNOS）蛋白表达的影响。方法：50只雄性SD大鼠随机分为假手术组（sham）、脑缺血再灌注模型组（MCAO）、预适应组（MCAO＋preconditioning）、后适应组（MCAO＋postconditioning）和尼莫地平组（MCAO＋nimodipine），每组10只大鼠。预适应组大鼠在MCAO前24h，双侧颈总动脉夹闭2min，再灌注20min，循环两次。后适应组大鼠在脑缺血再灌注开始时，再灌注20s，栓塞20s，循环3次。大鼠大脑中动脉阻断1．5h，再灌注24h。用TUNEL法和免疫组化染色法分别检测缺血半暗带凋亡细胞和iNOS、eNOS蛋白表达。结果：与MCAO组比较，后适应组大鼠脑缺血半暗带的凋亡细胞显著减少，eNOS蛋白表达显著增加，iNOS蛋白表达显著减少，差异有统计学意义（P〈0．05）。结论：缺血后适应能诱导脑缺血耐受，对脑缺血／再灌注损伤产生保护作用，其保护作用与促进eNOS蛋白的表达，抑制iNOS蛋白的表达有关。

Effect of ischemic postconditioning on neurocyte apoptosis and expression of eNOS and iNOS protein in cerebral ischemic reperfusion injury rats

AIM: To investigate the effects of postconditioning on neuron apoptosis and expression of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) protein in local cerebral ischemic reperfusion rats via middle cerebral artery occlusion (MCAO). METHODS: Fifty male Sprague-Dawley rats were randomized into five groups (n=10, each group), sham-operated group, MCAO group, preconditioning combined MCAO group, postconditioning combined MCAO group and nimodipine combined MCAO group. In the preconditioning groups animals were subject to 2 cycles of 2-min ischemia and 20-min reperfusion of the bilateral carotid arteries 24 h before middle cerebral artery occlusion. In the postconditioning groups animals were subject to 3 cycles of 20-second ischemia and 20-second reperfusion of the MCAO before reperfusion. At the 24th hour after reperfusion, the rat brains were obtained for detecting eNOS and iNOS protein expression by immunohistochemistry method. RESULTS: In the postconditioning groups, the apoptotic cells were significantly decreased (P< 0.05 ); the expression of eNOS protein was significantly increased (P< 0.05 ); on the contrary, that of iNOS protein was significantly decreased (P< 0.01 ). CONCLUSION: The postconditioning can prevent apoptosis in local cerebral ischemic reperfusion model rats due to the enhanced expression of eNOS protein and decreased expression of iNOS protein.