脑室内注射胰岛素改善心肺复苏后大鼠神经功能及其机制的研究

Study on the mechanism of intraventicular administration of insulin improve the cardiopulmonary resuscitation rats' neurological function

目的：观察脑室内注射胰岛素对心肺复苏（CPR）后大鼠海马CA1区神经元Caspase-3mRNA表达、神经元凋亡及神经功能的影响。方法：将30只雄性SD大鼠随机分为对照组、复苏组及胰岛素组,并采用室颤法制备大鼠CPR模型。结果：①大鼠CPR后24 h和72 h胰岛素与复苏组相比胰岛素抑制促凋亡基因Caspase-3 mRNA表达,胰岛素与复苏组Caspase-3基因表达分别为（CPR 24 h）0.43±0.03,1.39±0.36,P=0.01;（CPR 72 h）0.63±0.06,1.08±0.05,P=0.001;②大鼠CPR后7 d,胰岛素组凋亡细胞计数（92.79±7.50/mm2）明显低于复苏组凋亡细胞计数（124.75±17.35/mm2）（F=5.853,P=0.02）;③大鼠CPR后24 h,胰岛素组神经功能评分明显高于复苏组[（70（64-72）,56（50-58）;P〈0.001]。结论：胰岛素抑制CPR后大鼠神经元Caspase-3mRNA的表达,从而抑制神经元凋亡,改善神经功能,保护神经系统。

Objective： To explore the effect of intraventricular administration of insulin on proapoptotic expression of Caspase-3 mRNA and neuronal apoptosis in hippocampus CA1, and neurological function after rats＇ CPR. Methods： Thirty male SD rats were randomly divided intothree groups： sham group; the resuscitation with saline-treated group and resuscitation with insulin-treated group. Six minute cardiac arrest was induced by ventricular fibrillation（VF） via pacing electrode placed in rats＇ esophagus in saline and insulin group. Results： 1. The NDS revealed a clear neurological deficit after reperfusion 24 h, 72 h in insulin and saline group as compare to the sham group, Comparing to the saline group, Insulin could improve the rats＇ neurologic function after CPR 24（insulin vs. saline group, 70（64-72）vs.56（50-58）, P〈0.001）; 2. Through TUNEL stain, insulin inhibited apoptosis in CA1 hippocampus as compare to the saline after CPR 7d.（F=5.853, P=0.02） 3.Caspase-3 expression in insulin-treated groups were significantly decreased compared to the saline-treated group after reperfusion 24h and 72h[（70（64-72）, 56（50-58）; P〈0.001]. Conclusion： Intraventricular administration of insulin could inhibit the mRNA expression levels of the apoptotic activities of Caspase-3 after cardiac arrest, prevent neuronal apoptosis in the CA1 hippocampus and improve the rats＇ neurological function（at least 24hours） after CPR.