摘要
目的 :探讨促红细胞生成素 (Erythropoietin ,EPO)预处理的神经保护机制。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(rHu -EPO) 5μl,生理盐水组则给予等体积生理盐水 ,假手术组只进行假手术处理。观察缺血后 2 4h海马CA1区bcl -xl蛋白表达和缺血后 72h细胞凋亡。结果 :缺血后 2 4h ,EPO组海马CA1区bcl -xl蛋白表达与假手术组比较有显著差异 (P <0 .0 1) ,较生理盐水组表达增强 (P <0 .0 1)。缺血后 72h ,EPO组海马CA1区较生理盐水组有较少的凋亡细胞 (P <0 .0 1)。结论 :EPO预处理减少缺血海马细胞凋亡 ,促进bcl
Objective: Investigating neuroprotection mechanism of erythropoietin(EPO)when administered before global brain ischemia. Methods: Using 4-VO technique, we made the transient global brain ischemia model. Male Sprague-Dawley rats were randomized into sham operation group and physiological saline group and erythrop oietin group. 3 hours before global brain ischemia rHu-EPO(5 μl)was injected into lateral ventricles of rats by means o f stereospecific technology in EPO group, and physiological saline(5 μl)was injected in phy siological saline group, while the rats were only operated but their arteries were not occluded in sham operation group. Chan ges of bcl-xl protein expression were observed at 24 hours after global brain ischemia, and apoptosis were checke d at 72 hours in hippocampal CA1 subregion.Results:There was obvious difference in the expression of bcl-xl protein in hippocampal CA1 subregion between EPO group and sham operation group (P<0.01), but they were obviously more in both groups than that in physiological saline g roup (P<0.01) 24 hours after global brain ischemia. There were less apoptotic cells (P<0.01) in EPO group than that in physiological saline group 72 hours after global brain ischemia. Conclusion:EPO could inhibit apoptos is of neurons in hippocampal CA1 subregion when administrated before global brain ischemia, and up-regulating bcl-xl expression might contribute to t he protective mechanism.
出处
《西北国防医学杂志》
CAS
2004年第1期45-47,F003,共4页
Medical Journal of National Defending Forces in Northwest China
