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作 者:崔刚[1] 信照亮[1] 杨庆余[1] 周任[1] 屈建强[1]
机构地区:[1]西安交通大学第二医院神经外科,西安710004
出 处:《广州医药》2003年第6期9-11,共3页Guangzhou Medical Journal
摘 要:目的 :探讨纳洛酮对脑缺血再灌注的神经保护机制。方法 :采用线栓法制造的大鼠局灶性脑缺血再灌注模型 ,通过免疫组化法检测脑缺血不同再灌时间FOS蛋白的表达以及经纳洛酮 (5mg/kg)预处理后对该蛋白表达的影响。结果 :脑缺血 30min再灌 6hFOS蛋白表达显著增加 ,2 4h后基本降低到正常 ;纳洛酮可显著抑制脑缺血后FOS蛋白的表达。结论 :作为阿片肽受体拮抗剂 ,纳洛酮的神经保护机制可能与抑制cObjective: Investigate the neuroprotective mechanism of naloxone on cerebral ischemia reperfusion Methods: The model of cerebral ischemia reperfusion in rats was made by suture occluded method,the expression of FOS protein and the effect of naloxone (5mg/kg) applied prior ischemia on the expression were detected by immunohistochemical method at the different ischemia reperfusion time Results: The expression of FOS protein significantly increased after 30min ischemia followed by 6h reperfusion,then nearly decreased to normal after 24h Naloxone significantly inhibited the expression of FOS protein Conclusion: The neuroprotective mechanism of naloxone which is an opioids receptor antagonist is probably related to the inhibition of c fos gene expression
分 类 号:R743.3[医药卫生—神经病学与精神病学]
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