大鼠心脏骤停后行心肺复苏对海马脑组织的影响及机制

Effect of cardiopulmonary resuscitation on hippocampal brain after cardiac arrest in rats and its mechanism

目的探讨大鼠心脏骤停后,实施心肺复苏术对大鼠海马脑组织的保护作用和机制。方法SD大鼠40只,随机均分为对照组、缺血组、心肺复苏组、依达拉奉治疗组,采取窒息法使大鼠心脏骤停造模,缺血组大鼠心脏停跳10 min;复苏组实施心脏骤停/心肺复苏(CA/CPR),即使大鼠心脏停跳3 min后,再行心肺复苏7 min。10 min后处死各组大鼠,留取静脉血检测氧化应激指标,HE染色和电镜观察海马脑组织结构改变,实时荧光定量PCR和Western blot检测大鼠海马中Nrf2、Keap1基因和蛋白表达。结果与对照组大鼠比较,缺血组大鼠血清氧化应激水平升高,海马内神经细胞尼氏体减少,线粒体嵴破坏,Nrf2、Keap1基因和蛋白表达增加;与缺血组比较,心肺复苏组大鼠血清氧化应激水平降低,海马内神经细胞尼氏体增多,线粒体嵴破坏减轻,Nrf2、Keap1基因和蛋白表达降低。结论心脏骤停后心肺复苏术对大鼠海马脑组织具有保护作用,其机制与改善氧化应激损伤Nrf2/Keap1通路有关。

Aim To investigate the protective effect of cardiopulmonary resuscitation(CPR)on hippocampal brain tissues of rats after cardiac arrest and its mechanism.Methods Forty SD rats were randomly divided into control group,ischemia group,cardiopulmonary resuscitation group and Edaravone treatment group.The rats in ischemia group were subjected to cardiac arrest by suffocation for 10 min.In resuscitation group,cardiac arrest/cardiopulmonary resuscitation(CA/CPR)was performed,after 3 min of cardiac arrest,cardiopulmonary resuscitation was performed for 7 min.After 10 min,the rats in each group were sacrificed,venous blood was taken to detect oxidative stress indicators,and the pathology of rat hippocampal brain tissues were examined by HE staining and electron microscopy,and the expressions of Nrf2 and Keap1 gene and proteins were detected by real-time fluorescent quantitative PCR and Western blot.Results Compared with control group,the serum oxidative stress level of the ischemic model group rats increased,the Nissl body of the hippocampal nerve cells decreased significantly,the mitochondrial cristae were destroyed significantly,and the expressions of Nrf2 and Keap1 genes and proteins in the hippocampal tissues increased.Compared with ischemic group,the serum oxidative stress level of resuscitation group rats decreased.Compared with ischemic group,the serum oxidative stress level of the rats in cardiopulmonary resuscitation group decreased,the neuronal cells in the hippocampus increased,the mitochondrial cristae damage was alleviated,and the expressions of Nrf2 and Keap1 genes and proteins in the hippocampus decreased.Conclusions CPR has protective effect on hippocampal tissues of rats,and its mechanism is related to the alleviation of Nrf2/Keap1 pathway of oxidative stress injury.