促红细胞生成素对缺氧缺血性脑损伤保护作用机制的研究  

Protective mechanism of erythropoietin on hypoxic-ischemic brain damage

作　　者：张秋月[1] 陈国萍[1] 韩钢[1] 肇颖新[1] 

机构地区：[1]哈尔滨医科大学附属第一医院新生儿科,黑龙江哈尔滨150001

出　　处：《哈尔滨医科大学学报》2012年第6期559-560,565,共3页Journal of Harbin Medical University

基　　金：黑龙江省教育厅科学技术研究项目(11531161)

摘　　要：目的探讨促红细胞生成素对新生鼠缺氧缺血性脑损伤的保护作用机制。方法选用7日龄Wistar大鼠54只,分成假手术组、生理盐水对照组及促红细胞生成素治疗组,制备缺氧缺血性脑损伤(hypoxic-ischemic brain damage,HIBD)模型后分别给予不同的处置于24 h、48 h、72 h处死。检测脑组织中超氧化物歧化酶(SOD)、丙二醛(MDA)水平。结果盐水对照组SOD水平低、MDA水平高,同假手术组比较有显著性差异,促红细胞生成素治疗组SOD水平高、MDA水平低,同盐水对照组比较有显著性差异。结论促红细胞生成素可通过调节SOD活性,减少氧自由基所致损伤。这可能是其对缺氧缺血性脑损伤的保护作用机制之一。Objective hypoxicisehemic brain To investigate of the protective mechanism in erythropoietin （EPO）on damage of neonatal rats. Methods Fiftyfour Wistar rats at the age of 7dayold were divided into three groups, including normal group, HIBD groups, and EPO treatment group. After the model of HIBD was established, rats were killed at 24 h, 48 h, and 72 h respectively. Then the activity of superoxide dismutase （SOD） and the content of malond ialdehyde （MDA） in brain tissues were detected correspondingly. Results Lower SOD activi ty and higher MDA content were showed in HIBD groups when compared with normal group from rats. Moreover, there were significantly higher SOD activity and lower MDA content ap peared in EPO treatment on normal group than those in HIBD groups. Conclusion poietin can reduce the level of oxygen free radicals caused form injury by of SOD,which may be one of protective mechanisms on hypoxicischemic regulating Erythro the activity brain damage

关 键 词：促红细胞生成素 缺氧缺血性脑损伤 超氧化物歧化酶 丙二醛 

分 类 号：R332[医药卫生—人体生理学]