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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 被引量:11

Study on expression of caspase-3 and free radical injury in hypoxic-ischemic brain damage of neonatal rats
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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.
出处 《中国免疫学杂志》 CAS CSCD 北大核心 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)
关键词 缺氧缺血性脑损伤 半胱天冬酶-3 自由基 大鼠 新生 Hypoxic-ischemic brain damage Caspase-3 Free radical Neonatal rat
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