促红细胞生成素对心肺复苏后大鼠脑保护的研究与PI3K/AKT信号通路的相关性

Effect of Erythropoietin on Brain Protection in Rats after Cardiopulmonary Resuscitation and Its Correlation with PI3K/Akt Signaling Pathway

目的:是探讨促红细胞生成素(EPO)对心肺复苏后大鼠脑保护的作用疗效和促红细胞生成素是否可以通过磷脂酰肌醇3激酶/蛋白激酶B(PI3K/AKT)信号通路对大鼠心肺复苏后具有脑保护作用。方法:将60只健康雄性大鼠随机分为实验组和对照组,全部氯化钾致颤(10%kcl 0.3m L/kg脉冲式静脉注射诱发心搏骤停),立即行心肺复苏及气管插管等治疗,实验组给予促红细胞生成素,对照组给与同等量的生理盐水。观察不同时间点神经功能缺损评分;免疫组织化学染色观察半胱氨酸水解酶-3(caspase-3)、磷酸化蛋白激酶B(p-AKT)的表达;用HE染色方法观察脑组织受损情况。结果:实验组与对照组比较,caspase-3阳性细胞表达数量相对减少(P<0.05),p-AKT阳性细胞表达数量相对增加(P<0.05);实验组与对照组比较,神经细胞排列较整齐,细胞变形数量减少,细胞受损相对减轻。结论:促红细胞生成素对心肺复苏后大鼠具有脑保护作用,其机制可能与PI3K/AKT信号通路激活,抑制细胞凋亡有关,降低神经功能缺损评分,减轻神经元病理形态的损伤。

Objective: To investigate the effect of erythropoietin(EPO) on brain protection in rats after cardiopulmonary resuscitation(CPR) and whether EPO can protect the brain through the PI3 K/AKT signaling pathway. Methods: 60 healthy male rats were randomly divided into experimental group and control group. All potassium chloride induced fibrillation(10 % KCl 0.3 mL/kg pulse intravenous injection to induce cardiac arrest), and cardiopulmonary resuscitation and endotracheal intubation were immediately performed. The experimental group was given erythropoietic hormone, and the control group was given the same amount of normal saline. The neurological deficit scores at different time points were observed. The expression of caspase-3 and phosphorylated protein kinase B(p-Akt)were observed by immunohistochemical staining.He staining was used to observe the damage of brain tissue. Results: Compared with the control group, the expression of Caspase-3 positive cells decreased(P< 0.05), the expression of p-Akt positive cells was increased(P< 0.05);Compared with the control group,the nerve cells were arranged neatly, the number of cell deformation was reduced, and the damage of cells was relatively reduced. Conclusions: Erythropoietin can protect the brain of rats after cardiopulmonary resuscitation, and the mechanism may be related to the activation of PI3 K/Akt signaling pathway, inhibition of cell apoptosis, reduction of neurological deficit score and reduction of pathological morphological damage of neurons.