摘要
目的探讨大鼠局灶性脑缺血2h再灌注48h诱导型一氧化氮合酶(induciblenitricoxidesynthase,iNOS)来源的一氧化氮(nitricoxide,NO)对神经元凋亡的影响。方法闭塞大鼠左侧大脑中动脉造成局灶性脑缺血模型,给予选择性iNOS抑制剂氨基胍,硝酸还原酶法检测NO含量,流式细胞术检测硝基酪氨酸表达,应用末端转移酶介导的缺口末端标记法(TdTmediateddUTPnickendinglabelling,TUNEL)及流式细胞术检测缺血2h再灌注48h细胞凋亡的变化。结果氨基胍可使缺血2h再灌注48h大鼠脑内TUNEL阳性细胞明显减少,细胞凋亡百分率降低,凋亡峰降低。结论iNOS来源的NO参与介导脑缺血再灌注晚期的细胞凋亡。
ObjectiveTo investigate the effects of iNOS-derived NO on apoptosis following focal cerebral ischemia and reperfusion in rats. MethodsFocal cerebral ischemic model was induced by the occlusion of left middle cerebral artery. Aminoguandine, a selective inhibitor of iNOS, was given intraperitoneally. The rats were sacrificed at 48 h of reperfusion after 2 h of ischemia. The content of NO was measured by nitriate reductase method.The expression of NT was examined by flow cytometry.The cellular apoptosis was examined by flow cytometry and TUNEL. ResultsThe number of TUNEL positive cells and the apoptotic percentage were decreased markedly in Aminoguandine groups. ConclusioniNOS-derived NO may play a role in apoptosis following focal cerebral ischemia and reperfusion.
出处
《河北医科大学学报》
CAS
2005年第4期241-244,253,共5页
Journal of Hebei Medical University
关键词
脑缺血
脱噬作用
一氧化氮
大鼠
cerebral ischemia
apoptosis
nitric oxide
rats
