新生大鼠缺氧缺血性脑损伤后细胞凋亡与自由基损伤机制研究  

Study on the Mechanism of Cell Apoptosis and Free Radical Injury of Hypoxic-ischemic Brain Damage in Neonatal Rats

作　　者：黄广[1] 肖育 陈映曼[1] 

机构地区：[1]汕头大学医学院第一附属医院儿科,广东汕头515041 [2]广东省汕头市金平区人民医院急诊科,广东汕头515041

出　　处：《河北医学》2008年第3期255-258,共4页Hebei Medicine

摘　　要：目的：探讨新生大鼠缺氧缺血脑损伤（HIBD）后细胞凋亡与自由基损伤机制的研究。方法：7日龄SD大鼠72只，随机分成6组：①正常对照组；②HIBD后Oh组；③HIBD后24h组；④HIBD后48h组；⑤HIBD后72h组；⑥HIBD后7d组。制备HIBD模型后0，24，48，72h，7d后处死大鼠，取脑并检测脑组织中超氧化物歧化酶（SOD）、丙二醛（MDA）水平；并作HE和Tunel染色光镜下检测各组脑细胞凋亡数。结果：HIBD后各组脑组织SOD，MDA水平及脑细胞凋亡数与对照组比较均有显著性差异，48h及72h组与其他组比较有显著性差异；48h与72h组之间比较无显著性差异。结论：新生大鼠HIBD后48～72h为脑损伤高峰期，细胞凋亡与自由基损伤均参与了缺氧缺血后神经细胞的损害，阻止细胞凋亡或抗自由基损伤应争取在48h内进行。Objective： To investigate the mechanism of cell apoptosis and iree radical injury of hypoxicischemic brain damage （ HIBD ） in the newborn rats. Method： The 7 - day - old SD rats were subjected to control group, 0 hour after HIBD group, 24 hours after HIBD group, 48 hours after HIBD group.72 hours after HIBD group and 7days after HIBD group. The apoptosis cells of cortex was detected by terminal deoxynucleotidyl transferase mediated dUTP - biotin nick end labeling （ TUNEL ） staining. The content of MDA and SOD were observed at the same time. Result： The content of MDA and SOD, the pathologic changes and cell apoptosis are significantly different between the HIBD groups and the control group, There were significant difference between the 48 hours after HIBD group, 72 hours after HIBD group and other groups. There were no significant difference between the 48 hour after HIBD group and 72 hours after HIBD group . Conclusion： Cell apoptosis and free radical injury are the main mechanism of hypoxic-ischemic brain damage in the newborn rats. 48 to 72 hour is the crest-time of brain injury after HIBD, So prohibit cell apoptosis and anti-free radical must be done within 48 hours.

关 键 词：脑缺氧 脑缺血 细胞凋亡 自由基 

分 类 号：R722.1[医药卫生—儿科]