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出 处:《江苏医药》2015年第16期1877-1880,共4页Jiangsu Medical Journal
摘 要: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 explore the protective effect and underlying mechanism of recombinant human erythropoietin(rHuEPO) against status epilepticus(SE)‐induced neuron apoptosis in rats .Methods Sixty SD rats were equally divided into 5 groups .Group A was taken as blank control .SE models were established by kainic acid(KA) in the other 4 groups .Group B was taken as model control .Group C was treated with rHuEPO ,group D was treated with rHuEPO and LY294002 , and group E was treated with DMSO(a solvent of LY294002) .The protein expressions of Akt ,p‐Akt , Bcl‐2 and Bax were detected by Western blot .The mRNA expressions of Bcl‐2 and Bax were detected by qRT‐PCR .Results Bcl‐2 mRNA expression was higher in group C than that in group B (P〈0 .05) .The expression of p‐Akt protein was less in group D than that in group C (P〈0 .05) . Conclusion The rHuEPO has a neuroprotective effect on SE‐induced neuron apoptosis in rats .The mechanism for that may be through PI3K/AKT pathway to regulate the expressions of Bcl‐2 and Bax , which mediates mitochondrial apoptotic pathways and inhibits cell apoptosis .
分 类 号:R322[医药卫生—人体解剖和组织胚胎学]
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