脑活素治疗新生大鼠缺血缺氧性脑病机理的研究

Study on the Mechanism of Treatment Effects of Cerebrolysin on Hypoxic - ischemic Encephalopathy of Neonatal Rat

7日龄Wister大鼠结扎左侧颈总动脉后吸入氧氮混合气体（8％O2和92％N2）2h,制成缺血缺氧性脑病动物模型,测定大鼠脑组织中丙二醛（MDA）的含量和超氧化物歧化酶（SOD）的活性。结果显示,缺血缺氧后6h,缺血缺氧组MDA含量显著升高,24h达到高峰,以后逐渐下降,96h与对照组比较无统计学差异;缺血缺氧脑活素治疗组MDA含量于缺血缺氧后6h已经显著下降,72h与对照组比较无统计学差异。缺血缺氧组SOD活力值在缺血缺氧后6h已经下降,24h降到最低点,以后逐渐回升,96h与对照组比较无统计学差异;缺血缺氧脑活素治疗组SOD活力值在缺血缺氧后6h明显提高,于缺血缺氧后96h与对照组比较无统计学差异。结果提示,缺血缺氧引起新生大鼠脑组织的氧化-抗氧化系统失衡,氧自由基大量产生,参与了新生大鼠缺血缺氧性脑病脑损伤过程;脑活素能够抑制氧自由基的生成,提高SOD的活力值,对缺血缺氧性脑病具有神经保护作用。

Wister rats of 7 - old day underwent unilateral common carotid artery ligation and exposure to hypoxic state (8 % oxygen + 92 % nitrogen ) and newborn- rat hypoxic- sichemic encephalopathy(HIE) model was set . The content of malon dialdehyde (MDA) and the activity of superoxide dismutase (SOD) in the brain tissue of rats were measured . The results showed that the content of MDA of the hypoxic- ischemic (HI) group had significantly increased at 6 hour after HI and was the highest at 24 hour and slightly higher than that of the control group(P> 0. 05) at 96 hour ; the content of MDA of the HI cerebrolysin- treated group had significantly discreased at 6 hour after HI and then returned to the same level of as that of the control group (P>0.05)at 72 hour . The activity of SOD had discreased at 6 hour after HI and was the lowest at 24 hour and then graduly rised again to the level of the control group(P>0. 05) at 96 hour;the activity of SOD of HI cerebrolysin-treated group had significantly increased at 6 hour after HI and returned to the same level as that of the control group(P>0. 05) at 96 hour . The results suggested that the excessive oxygen free radicals participated the brain damages of neonatal rat after HI and cerebrolysin had the treatment effects on HIE by restraining the produce of the oxygen free radicals and increasing the activity of SOD.