大鼠脑缺血再灌注中iNOS源性NO/ONOO^-对Caspase-1蛋白表达的影响  

EFFECTS OF iNOS-DERIVED NO/ONOO^-ON CASPASE-1 PROTEIN EXPRESSION FOLLOWING FOCAL CEREBRAL ISCHEMIA AND REPERFUSION IN RATS

作　　者：赵昱[1] 尹青[1] 王立轩[1] 罗波 张爱子[1] 马洪骏[1] 李陈莉[1] 

机构地区：[1]河北医科大学基础医学院组织胚胎学教研室,河北石家庄050017 [2]石家庄市裕华区裕华西路卫生院,河北石家庄050000

出　　处：《河北医科大学学报》2006年第3期161-163,184,共4页Journal of Hebei Medical University

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。Objective To 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. Methods Focal 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 expressi,on of nitrotyrosine was examined by flow cytometry. The Caspase-1 expression was detected immunohistochemically. Results The expression of Caspase-1 protein was remarkably lower in aminoguandine groups than vehicle group. Conclusion NO/ONOO- derived from iNOS might promote apoptosis following focal cerebral ischemia and reperfusion via upregulating Caspase-1 expression.

关 键 词：脑缺血 细胞凋亡 基因表达 

分 类 号：R743.34[医药卫生—神经病学与精神病学]