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大鼠脑缺血再灌注中iNOS源性NO/ONOO-对Caspase-1蛋白表达的影响
引用本文:赵昱,尹青,王立轩,罗波,张爱子,马洪骏,李陈莉.大鼠脑缺血再灌注中iNOS源性NO/ONOO-对Caspase-1蛋白表达的影响[J].河北医科大学学报,2006,27(3):161-163,184.
作者姓名:赵昱  尹青  王立轩  罗波  张爱子  马洪骏  李陈莉
作者单位: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;石家庄市裕华区裕华西路卫生院,河北,石家庄,050000
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.

关 键 词:脑缺血  细胞凋亡  基因表达
文章编号:1007-3205(2006)03-0161-03
收稿时间:2006-01-25
修稿时间:2006-01-25

EFFECTS OF iNOS-DERIVED NO/ONOO- ON CASPASE-1 PROTEIN EXPRESSION FOLLOWING FOCAL CEREBRAL ISCHEMIA AND REPERFUSION IN RATS
ZHAO Yu,YIN Qing,WANG Li-xuan,LUO Bo,ZHANG Ai-zi,MA Hong-jun,LI Chen-li.EFFECTS OF iNOS-DERIVED NO/ONOO- ON CASPASE-1 PROTEIN EXPRESSION FOLLOWING FOCAL CEREBRAL ISCHEMIA AND REPERFUSION IN RATS[J].Journal of Hebei Medical University,2006,27(3):161-163,184.
Authors:ZHAO Yu  YIN Qing  WANG Li-xuan  LUO Bo  ZHANG Ai-zi  MA Hong-jun  LI Chen-li
Institution:1. Department of Histology and Embryology, the School of Basic Medical Science, Hebei Medical University, Shijiazhuang 050017, Cnina ;2. Public Health Centre of Yuhua West Road in Yuhua District Shijiazhuang City, Shijiazhuang 050000, Cnina
Abstract: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.
Keywords:brain ischemia  apoptosis  gene expression
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