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机构地区:[1]大连医科大学附属第二医院神经内科,辽宁省大连市116027
出 处:《中华全科医学》2009年第9期907-909,F0003,共4页Chinese Journal of General Practice
摘 要:目的观察大鼠脑缺血再灌注后细胞凋亡相关Fas-L蛋白的变化,进一步探讨脑缺血再灌注后细胞凋亡机制及尤瑞克林的脑保护作用。方法线栓法制作脑缺血再灌注模型,分别对假手术组、脑缺血再灌注组(2h组、6h组、12h组、24h组、48h组、72h组)、尤瑞克林干预组以及生理盐水对照组,采用免疫组化方法观察测定各组大鼠脑内的Fas-L的表达情况并进行神经功能缺损评分。结果脑缺血再灌注组与假手术组比较,各时间点Fas-L蛋白均表达增多(P<0.05),脑缺血再灌注6h组Fas-L蛋白表达达高峰(P<0.05)。尤瑞克林干预组与生理盐水对照组比较Fas-L蛋白表达减少(P<0.01)。结论尤瑞克林对脑缺血再灌注有明显的保护作用,抑制Fas-L蛋白表达可能是其对脑缺血再灌注损伤起保护作用的分子机制之一。Objective To investigate the brain protecting mechanism of Urinary Kallidinogenase and offer the theoretical basis for clinical therapy of ischemia cerebrovascular disease. Methods SD rat was used as a model of focal cerebral ischemia and reperfusion to observe expression of Fas-L protein on every time after focal cerebral ischemia-reperfusion and the protective func- tion of Urinary Kallidinogenase. Immunohistochemical method were used to measure the number of Fas-L positive ceils in rat' s cerebral cortex of sham-operated group,model group and Urinary Kallidinogenase group. Results Fas-L protein had a low-level expression and increased significantly after ischemia reperfusion (P 〈 0.05 ) , peaked at 6 h after reperfusion. The Urinary Kallidinogenase can significantly reduce the expression of the Fas-L protein( P 〈 0.01). Conclusion The Urinary Kallidinogenase had obviously protective function for ischemia-reperfusion rat.
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