摘要
目的探讨促红细胞生成素在脑缺血再灌注损伤中的保护作用及其可能的机制。方法采用Zea Longa改良线栓法制作局灶性大鼠脑缺血再灌注损伤模型。取健康成年雄性SD大鼠60只,随机分为正常组、假手术组、缺血再灌注组和EPO干预组,每组15只大鼠。EPO干预组分别于缺血前2h、缺血后6h、缺血后24h予以EPO 3000 IU/kg腹腔注射。缺血再灌注组、假手术组和正常组于相应时间给与等量生理盐水。再灌注72h后进行神经功能缺损评分,检测Nissl小体、脑红蛋白(NGB)和单核细胞趋化蛋白-1(MCP-1)的表达。结果与缺血再灌注组比较,EPO干预组的神经功能明显改善。EPO干预组Nissl小体减少的程度较轻。EPO干预组的NGB表达明显高于缺血再灌注组(P<0.01);而EPO干预组的MCP-1表达明显低于缺血再灌注组(P<0.01),均以缺血前2hEPO干预亚组明显。结论EPO可能通过上调NGB和下调MCP-1表达而减轻脑缺血再灌注损伤。
Objective To investigate protection of erythropoietin （EPO） against cerebral ischemia-reperfusion injury in rats and possible mechanisms. Methods The model of focal cerebral ischemia-reperfusion injury was prepared by occluding middle cere- bral artery. Sixty male adult SD rats were randomly divided into four groups （n = 15 each） ： normal, sham-operated, ischemia- reperfusion and EPO-treated. The EPO treated group received an intraperitoneal injection of rHu-EPO （ 3000 IU/kg） 2 hrs before and 6 hrs and 24 hrs after cerebral ischemia, while the other three groups received the same volume of normal saline. Neurologi- cal deficit scores were evaluated and the expression of Nissl body, neuroglobin （NGB） and monocyte chemoattractant protein-1 （ MCP-1 ） was detected. Results EPO treatment resulted in an obvious improvement in neurological function. The expression of Nissl body in the EPO-treated group was significantly higher than that in the ischemia-reperfusion group （ P 〈 0.01 ）. The expression of NGB increased, while the MCP-1 expression decreased significantly in the EPO-treated group compared with that in the ischemia-reperfusion group （P 〈 0.01 ）. The most significant differences were observed between the EPO pre-treatment （2 hrs before ischemia） subgroup and the iscbemia-reperfusion group. Conclusions EPO may alleviate cerebral ischemia-reperfusion injury in rats, possibly through increasing NGB expression and decreasing MCP-I expression.
出处
《国际神经病学神经外科学杂志》
2009年第5期391-394,共4页
Journal of International Neurology and Neurosurgery
