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目的探讨重组人红细胞生成素(rHuEPO)对大鼠癫痫持续状态(SE)诱导的神经元凋亡的保护机制。方法 SD大鼠60只随机均分为五组:A组为空白对照;其余四组采用海人酸(KA)点燃大鼠SE模型后,B组作为模型对照,C组用rHuEPO处理,D组用rHuEPO和LY294002处理,E组用二甲基亚砜(LY294002的溶剂)处理。Western blot法检测Akt、p-Akt、Bcl-2和Bax蛋白表达;定量RT-PCR检测Bcl-2和Bax mRNA表达。结果 C组Bcl-2mRNA表达量高于B组(P<0.05),D组p-Akt蛋白表达低于C组(P<0.05)。结论 rHuEPO对SD大鼠SE诱导的海马神经元具有保护作用;其机制可能是通过PI3K/Akt途径对线粒体凋亡途径相关调控因子Bcl-2和Bax进行调控,进而介导线粒体凋亡途径,抑制细胞凋亡。
Objective To investigate the protective mechanism of recombinant human erythropoietin (rHuEPO) on neuronal apoptosis induced by epileptic seizure (SE) in rats. Methods Sixty Sprague-Dawley rats were randomly divided into five groups: group A was blank control; the other four groups were treated with kainate (KA), and group B was used as model control; group C was treated with rHuEPO; group D Treatment with rHuEPO and LY294002, group E was treated with dimethyl sulfoxide (solvent of LY294002). The protein expression of Akt, p-Akt, Bcl-2 and Bax were detected by Western blot and the mRNA expression of Bcl-2 and Bax by quantitative RT-PCR. Results The expression of Bcl-2 mRNA in group C was higher than that in group B (P <0.05). The expression of p-Akt in group D was lower than that in group C (P <0.05). Conclusions rHuEPO can protect the hippocampal neurons induced by SE in SD rats. Its mechanism may be through the PI3K / Akt pathway regulating the mitochondrial apoptosis-related regulatory factors Bcl-2 and Bax, and then mediating mitochondrial apoptosis pathway and inhibiting Apoptosis.