新生大鼠缺氧缺血性脑损伤caspase-3表达与自由基损伤机制的研究  

Study on expression of caspase-3 and free radical injury in hypoxic-ischemic brain damage of neonatal rats

作　　者：闫昆明[1] 刘英[2] 张芮[2] 郭世杰[2] 

机构地区：[1]长春生物制品研究所有限责任公司,长春130062 [2]吉林大学第一医院新生儿科,长春130021

出　　处：《中国免疫学杂志》2015年第8期1094-1097,共4页Chinese Journal of Immunology

基　　金：吉林省卫生厅科研项目资助(2013Z015)

摘　　要：目的:研究缺氧缺血性脑损伤(HIBD)新生大鼠caspase-3表达与自由基损伤的机制。方法:建立7日龄新生大鼠HIBD模型,分为HIBD组和假手术组,两组分别于HI后6、12、24、48、72、96 h取脑组织,应用TUNEL法检测神经细胞凋亡,免疫组织化学法检测caspase-3蛋白的表达,硫代巴比妥酸法测定丙二醛(MDA)含量,黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)含量。结果:HIBD组神经细胞凋亡数量及caspase-3的表达量6 h开始增多,48 h达高峰,各时间点两者均显著高于假手术组(P<0.05)。HIBD组MDA含量6 h增高,24 h达高峰,各时间点均较假手术组增高(P<0.05)。HIBD组SOD含量6 h下降,24 h降至最低,各时间点均较假手术组降低(P<0.05)。凋亡细胞数量与caspase-3蛋白表达量和MDA含量均呈正相关(r=0.748、0.654,P均<0.05),与SOD含量呈负相关(r=-0.576,P<0.05)。结论:HIBD时自由基损伤促进caspase-3的表达及神经细胞的凋亡。Objective： To study the expression of caspase-3 and free radical injury in hypoxic-ischemic brain damage（ HIBD）of neonatal rats. Methods： All seven-day-old Wistar rats were randomly divided into HIBD group and sham operation group. Brains was obtained at time of 6 h,12 h,24 h,48 h,72 h,96 h after HIBD. Neuronal cell apoptosis was detected by terminal deoxynucleotidyl transferase mediated d UTP-biotin nick end labeling（ TUNEL）. The expression level of caspase-3 protein was detected by immunohistochemistry. The level of malondialdehyde（ MDA） and supemxide dismutase（ SOD） were measured by thiobarbitic acid colorimetry and xanthin oxidase,respectively. Results： The number of neuronal cell apoptosis and the expression of caspase-3 protein began to increase at 6h and reached the peak at 48 h in HIBD group,they were both significantly higher than those in the sham operation group at each time point（ P〈0. 05）. The level of MDA began to increase at 6 h and reached the peak at 24 h in HIBD group,it was significantly higher than the sham operation group at each time point（ P〈0. 05）. The level of SOD began to decrease at 6 h and reached the lowest level at 24 h in HIBD group,it was significantly lower than the sham operation group at each time point（ P〈0. 05）. The number of neuronal cell apoptosis and the expression of caspase-3 protein were positively correlated with the level of MDA,but they were negatively correlated with the level of SOD. Conclusion： Free radical injury promotes the expression of caspase-3 and neuronal cell apoptosis in HIBD.

关 键 词：缺氧缺血性脑损伤 半胱天冬酶-3 自由基 大鼠 新生 

分 类 号：R332[医药卫生—人体生理学]