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目的探讨促红细胞生成素(Erythropoietin,EPO)的神经保护机制。方法采用4-VO法制作大鼠全脑缺血模型。将SD大鼠随机分为假手术组、生理盐水对照组、EPO预处理组。全脑缺血前3h,EPO组大鼠脑室立体定向注射重组人促红细胞生成素(rHu-EPO),生理盐水组则给予生理盐水,假手术组只进行假手术处理。观察缺血后24h各组海马CA1区bcl-xl和细胞色素C(CytochromeC,CytC)表达是否有相关性。结果bcl-xl和CytC预处理可以抑制缺血后大鼠海马CA1区神经元CytC从线粒体释放入胞浆,这种作用可能与促进bcl-xl表达相关。
Objective To investigate the neuroprotective mechanism of erythropoietin (EPO). Methods The rat model of global cerebral ischemia was made by 4-VO method. The SD rats were randomly divided into sham operation group, saline control group and EPO pretreatment group. Rats in the EPO group were injected stereotactically with recombinant human erythropoietin (rHu-EPO) 3 h prior to global cerebral ischemia. Rats in the physiological saline group were given normal saline. Sham-operated rats were sham-operated only. To observe whether the expression of bcl-xl and cytochrome C (CytC) in hippocampal CA1 region of each group after 24h of ischemia were correlated. Results Pretreatment with bcl-xl and CytC could inhibit the release of CytC from mitochondria into the cytoplasm of hippocampal CA1 neurons in ischemic rats. This effect may be related to the promotion of bcl-xl expression.