亚低温减少大鼠短暂性全脑缺血后皮质iNOS诱导的神经元凋亡

ATTENUATION OF iNOS-MEDIATED NEURONAL APOPTOSIS BY MILD HYPOTHERMIA AFTER TRANSIENT GLOBAL CEREBRAL ISCHEMIA IN RAT CEREBRAL CORTEX

为研究亚低温对大鼠脑缺血再灌注后皮质iNOS表达、NO产生及神经元凋亡的影响及探讨亚低温的神经保护机制,用大鼠短暂全脑缺血模型,采用Nissl染色观察存活神经元、免疫组化法检测iNOS、硝酸还原酶法检测NOx-水平和TUNEL染色结合电子显微镜观察检测凋亡神经元。结果显示:常温缺血组额叶皮质iNOS表达、NOx-水平增高,出现凋亡神经元;低温缺血组iNOS表达、NOx-水平明显低于常温缺血组,未检测到凋亡神经元。上述结果提示,脑缺血后iNOS来源的NO参与了神经元的凋亡过程,亚低温可减少大鼠短暂性全脑缺血后iNOS诱导的神经元凋亡。

The transient global cerebral ischemia was carried out in rats to explore the neuroprotective mecanism of mild hypothermia. The live neurons were counted by Nissl staining, the expression of iNOS protein was assessed by using immunohis-tochemical methods, the NO level was assessed by nitrate reductase methods, and apoptotic neurons were assessed by TUNEL staining and electron microscopy. The expression of iNOS and the NOx- level were increased, and apoptotic neurons were detected in norrnothermic ischemic frontal cortex. The expression of iNOS and the NOX- level were reduced, and apoptotic neuron was not detected in hyporhermic ischemic animals. These results suggest that iNOS-drived NO is implicated in the process of neu-ronal apoptosis after cerebral ischemia, and mild hypothermia attenuates iNOS-mediated neuronal apoptosis after trasient global ischemia in rat cerebral cortex.