Study on the mechanism of intraventicular administration of insulin improve the cardiopulmonary resuscitation rats’ neurological function
10.3969/J.ISSN.1672-8270.2014.06.005
- VernacularTitle: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
- Author:
Jingyu HE
;
Jing WANG
- Publication Type:Journal Article
- Keywords:
Cardiopulmonary resuscitation;
Insulin;
Caspase-3;
Apoptosis;
Neurological function;
SD rats were
- From:
China Medical Equipment
2014;(6):14-17,18
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the effect of intraventricular administration of insulin on pro-apoptotic 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 into three 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.
