促红细胞生成素预处理对大鼠脑缺血再灌注损伤的影响

目的研究促红细胞生成素（EPO）预处理对大鼠脑缺血再灌注损伤的影响。方法将30只SD大鼠随机分为3组：假手术组、模型组、干预组，每组10只。干预组给予EPO预处理，15min后，对模型组和干预组建立大脑中动脉栓塞模型，建模后2h进行血流再灌注；对假手术组仅建立假手术模型，建模后2h灌注生理盐水。记录各组大鼠神经功能缺陷评分、脑梗死面积、脑神经元凋亡情况，用RT-PCR检测谷氨酸转运体（GLT-1）mRNA的表达量，免疫组化法检测谷氨酸-天冬氨酸转运体（GLAST）蛋白表达。结果干预组大鼠神经功能缺陷评分和脑梗死灶面积明显小于模型组（P均〈0．05）。与假手术组比较，模型组大量神经细胞凋亡，而干预组缺血区仅部分凋亡。脑缺血再灌注后2h，模型组与干预组大鼠缺血区GLT-1 mRNA和GLAST蛋白表达均低于假手术组（P均〈0．05），而干预组表达水平明显高于模型组（P均〈0．05）。结论EPO预处理可减轻大鼠脑缺血再灌注损伤。

Effect of erythropoietin on the injury caused by cerebral ischemia/reperfusion in rats

Objective To investigate the protection effect of erythropoietin （EPO） pretreatment on the injury caused by cerebral ischemia / reperfusion in rats. Methods A total of 30 SD rats were randomly divided into three groups： sham-operated group, model group and intervention group. Rats in the intervention group were treated with EPO 15 minutes before modeling. The brain ischemia model was subsequently induced in all the groups except the sham-operated group. Two hours after modeling, the rats in the model and intervention groups subjected to ischemia / re-perfusion, and the rats in the sham- operated group were given the saline instead. Of all the rats, the rat neural function defect scores, cerebral infract areas nerve cell apoptosis were detected, glutamate transporter 1 （GLT- 1） mRNA expressions were determined by RT-PCR, and glutamate-aspartate transporter （GLAST） protein expressions were observed by immunohistochemistry. Results The levels of rat neural function defect score and cerebral infract areas were significantly lower in the intervention group than those in the model group （all P 〈 0.05）. The amount of nerve cells apoptosis decreased obviously in the intervention group compared with the model group.Expressions of GLT-1 mRNA and GLAST protein showed much higher in the intervention group than those in the model group 2 hours after cerebral ischemia/reperfusion （all P 〈 0.05）, but remarkably lower in both groups compard with the sham-operated group （all P 〈 0.05）. Conclusion EPO pretreatment could attenuate the injury caused by cerebral ischemia / reperfusion in SD rats.