重组人红细胞生成素对大鼠癫痫持续状态诱导的神经元凋亡的保护机制  被引量:1

Protective effect and mechanism of rHuEPO against status epilepticus-induced neuron apoptosis in rats

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作  者:潘振华 徐院花 田田 

机构地区:[1]南京上海梅山医院检验科,江苏省210039

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 .

关 键 词:重组人红细胞生成素 癫痫持续状态 细胞凋亡 

分 类 号:R322[医药卫生—人体解剖和组织胚胎学]

 

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