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大鼠局灶性脑缺血再灌注后fas基因和fasL基因表达变化的规律 被引量:3

Changes of fas and fasL gene expression in rats after focal cerebral ischemia reperfusion
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摘要 目的:探讨大鼠局灶性脑缺血再灌注后FasmRNA和FasLmRNA的表达变化。方法:实验于2004-03-01/06-30在哈尔滨医科大学附属第二医院科研中心进行。取健康Wister大鼠48只随机分为6组,即假手术组,缺血2h再灌注6,12,24,48和72h组,每组8只鼠。线栓法建立大鼠大脑中动脉闭塞(MCAO)及再通模型,应用RT-PCR技术检测MCAO及再通后缺血半暗带皮质FasmRNA和FasLmRNA表达。结果:假手术组FasmRNA,FasLmRNA均未见表达,再灌注6h起二者开始有少量表达(分别为0.23±0.02和0.06±0.01),FasmRNA的表达高峰在再灌注24h(0.94±0.06),FasLmRNA的表达高峰在再灌注48h(0.35±0.02),再灌注72h二者的表达均明显下降(分别为0.45±0.03和0.22±0.03)。结论:脑缺血再灌注可诱导FasmRNA和FasLmRNA表达。 AIM:To investigate the changes in the expression of Fas mRNA and FasL mRNA in rats after focal cerebral ischemia reperfusion. METHODS:From March 1st,2004 to June 30th,2004, the experiment was conducted in the Scientific Research Center,the Second Affiliated Hospital of Harbin Medical University.Forty eight Wistar rats were randomized into 6 groups: sham operated group, and 6 ,12 ,24 ,48,72 hour reperfusion after 2 hour ischemia groups.There were 8 rats in each group. Rat model of middle carotid artery occlusion(MCAO) and recanalization was made with thread ligation.Expression of Fas mRNA and FasL mRNA in the cortex of ischemic penumbral region was detected wth RT PCR technique. RESULTS:There were no expressions of Fas mRNA and FasL mRNA in the sham operated group.Six hours after reperfusion, the expression of Fas mRNA and FasL mRNA occurred(0.23±0.02 and 0.06±0.01,respectively) , their expression reached the peak respectively at 24 hours(0.94±0.06) and 48 hours(0.35±0.02) after reperfusion and both of them began to decrease at 72 hours after reperfusion(0.45±0.03 and 0.22±0.03 respectively). CONCLUSION:Cerebral ischemia reperfusion can induce the expression of Fasm RNA and FasL mRNA.
出处 《中国临床康复》 CAS CSCD 2004年第34期7692-7693,共2页 Chinese Journal of Clinical Rehabilitation
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  • 1Longa EZ, Weinstein PN, Carlson S, et al. Reversible middle cerebral artery occlusionWithout craniotomy in rats. Stroke 1989; 20(2) :84 - 91
  • 2Martin A, Herr I, Jeremias I, et al. CD95 ligand (Fas-L/APO-IL) and TNF-related apoptosis-inducing ligand mediate is-chemia-induced apoptosis in neurons. J Neurosci 1999; 19:3809 - 17

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