摘要
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、生理盐水组、EPO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 (recombinantHumanErythropoietin ,rHuEPO) ,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 2 4h海马CA1区细胞色素C(CytochromeC ,CytC)的变化 ,及缺血后 72h海马CA1区细胞凋亡情况。结果 EPO组海马CA1区呈现点状分布的CytC表达较生理盐水组增强 (P <0 .0 1) ,并且较生理盐水组呈现较少的凋亡细胞 (P <0 .0 1)。结论 EPO预处理可以抑制海马CA1区CytC从线粒体向胞浆释放及减少神经元凋亡。
Objective To explore the neuroprotection mechanism of erythropoietin(EPO). Methods Transient global cerebral ischemia model was made by four-vessel occlusion(4-VO)technique. Male Spraque-Dawley rats were the experimental objects and were randomly separated into 3 groups including Sham,Saline control and EPO-Pretreatment. At 3h before global cerebral ischemia,saline or recombinant Human Erythropoietin(rHuEPO)was respectively injected into the lateral ventricle of rat,with the help of stereotaxic coordinates,upon the designed conditions. The Sham rats were only performed the incision on cervix but without any treatment on the arteries. Expression of cytochrome c(CytC)was observed at 24h and neuronal apoptosis was checked at 72h after the model operation,in hippocampal CA 1 subregion. Results Hippocampal CA 1 subregion showed stronger expression of cytochrome c presenting punctual distribution but less cells of apoptosis in EPO group than in Saline group(P< 0.01). Conclusion Pretreatment of EPO could reduce the neuronal apoptosis but inhibit cytochrome c release into cytoplasm in hippocampal CA 1 subregion in the modeled rat.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2004年第3期222-224,i001,共4页
Journal of Apoplexy and Nervous Diseases
