缺血再灌注脑组织nNOS源性NO/ONOO-对Bcl-2表达的影响

目的 探讨大鼠局灶性脑缺血再灌注过程中神经元型一氧化氮合酶（nNOS）源的一氧化氮（NO）和过氧亚硝基阴离子（ONOO^-）对Bcl-2表达的影响。方法闭塞大鼠左侧大脑中动脉造成局灶性脑缺血模型，给予不同剂量选择性nNOS抑制剂7-硝基吲唑，用硝酸还原酶法检测脑组织一氧化氮（NO）水平，流式细胞术检测硝基酪氨酸（NT）表达，RT—PCR法检测Bcl-2表达的变化，并与溶剂对照组进行比较。结果 脑缺血再灌注损伤大鼠脑组织NO含量和NT表达下降，Bcl-2表达升高，且均呈剂量依赖性。结论 大鼠局灶脑缺血再灌注中，nNOS来源的NO／ONOO^-可下调Bcl-2表达并促进细胞凋亡的发生。

Effect of nNOS-derived NO/ONOO- on Bcl-2 expression following focal cerebral ischemia and reperfusion

[Objective] To investigate the effects of nNOS-derived NO/ONOO-on Bcl-2 mRNA expression following focal cerebral ischemia and reperfusion in rats. [Method] Focal cerebral ischemic model was induced by the occlusion of left middle cerebral artery. 7-nitroindazole, a selective inhibitor of nNOS, was given intraperitoneally. The rats were sacrificed at 6h of reperfusion after 2h of ischemia. The content of NO was measured by nitrate reductase method. The expression of NT were examined by flow cytometry. The Bcl-2 mRNA expression were detected by RT-PCR. [Result] The expression of Bcl-2mRNA was remarkably higher in 7-nitroindazole groups than that in vehicle group,the content of NO and the expression of NT were lower in 7-nitroindazole groups than those in vehicle groups. [Conclusion] NO/ONOO-derived from nNOS may promote apoptosis following focal cerebral ischemia and reperfusion via downregulating Bcl-2 expression.