【摘要】 目的探讨大鼠局灶性脑缺血2 h再灌注48 h诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)来源的一氧化氮(nitric oxide,NO)和过氧亚硝基阴离子(peroxynitrite,ONOO-)对Caspase-1蛋白表达的影响。方法闭塞大鼠左侧大脑中动脉造成局灶性脑缺血模型。给予选择性iNOS抑制剂氨基胍,采用硝酸还原酶法检测脑组织NO含量、流式细胞术检测硝基酪氨酸表达、免疫组织化学法检测Caspase-1蛋白表达的变化。结果与单纯缺血/再灌注组比较,腹腔注入氨基胍抑制iNOS活性可使Caspase-1蛋白表达降低。结论大鼠局灶脑缺血再灌注过程中,iNOS来源的NO/ONOO-可促进Caspase-1蛋白表达,这可能是iNOS活性增加促进细胞凋亡的机制之一。更多还原

【Abstract】 ObjectiveTo investigate the effects of iNOS-derived NO/ONOO~-on Caspase-1 protein expression following focal cerebral ischemia and reperfusion in rats which were sacrificed at 48 h of reperfusion after 2 h of ischemia.MethodsFocal cerebral ischemic model was induced by the occlusion of left middle cerebral artery.Aminoguandine,a selective inhibitor of iNOS,was given intraperitoneally.The content of NO was measured by nitriate reductase method.The expression of nitrotyrosine was examined by flow cytometry.The Caspase-1 expression was detected immunohistochemically.ResultsThe expression of Caspase-1 protein was remarkably lower in aminoguandine groups than vehicle group.ConclusionNO/ONOO~-derived from iNOS might promote apoptosis following focal cerebral ischemia and reperfusion via upregulating Caspase-1 expression.更多还原