Erythropoietin preconditioning suppresses neuronal death following status epilepticus in rats
Erythropoietin preconditioning suppresses neuronal death following status epilepticus in rats
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DOI：
10.55782/ane-2007-1641
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发表时间：
2007-01-01
影响因子：
1.4
通讯作者：
Deng, YanChun
中科院分区：
文献类型：
--
作者：
Yang, Jun;Huang, YuanGui;Deng, YanChun
癫痫持续状态（SE）是一种严重的疾病，其中大脑经历持续的癫痫发作，这可能导致神经元损失。我们以前的研究表明，促红细胞生成素（Epo）预处理通过抑制半胱氨酸蛋白酶-3（caspase-3）来抑制体内SE大鼠海马神经元的凋亡。在这项研究中，我们探讨了机制，Epo预处理可能发挥其抗凋亡作用，使用锂-匹罗卡品诱导的大鼠SE模型。Epo对神经元细胞死亡的影响使用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）进行了评估，Bcl-2蛋白家族的作用，已被证明是抗（Bcl-2，Bcl-w）或促（Bid，Bim）凋亡，用免疫荧光法进行了检查。Epo预处理后TUNEL、Bim和Bid阳性细胞总数减少，Bcl-2和Bcl-w阳性细胞总数增加。这些结果表明，全身性Epo预处理保护SE急性期的神经元，并可能通过调节促凋亡和抗凋亡Bcl-2家族蛋白之间的平衡，进一步抑制海马中的神经元凋亡。
Status epilepticus (SE) is a grave condition in which the brain undergoes lasting seizures which can lead to neuronal loss. Our previous study suggested that preconditioning with erythropoietin (Epo) Suppressed neuronal apoptosis in hippocampus of rats following SE in vivo by inhibiting caspase-3. In this study, we investigated the mechanisms by which Epo preconditioning may exert its anti-apoptotic effects using a lithium-pilocarpine induced SE model in rats. The effects of Epo on neuronal cell death were evaluated using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), and the role of the Bcl-2 protein family, which have been shown to be anti- (Bcl-2, Bcl-w) or pro- (Bid, Bim) apoptotic, was examined with immunofluorescence. We found Epo preconditioning decreased the total number of TUNEL, Bim and Bid positive cells, but increased the total number of Bcl-w and Bcl-2 positive cells. These results suggest that systemic Epo pretreatment protects neurons in an acute phase of SE and may result in further Suppression of neuronal apoptosis in hippocampus by regulating the balance between pro- and anti-apoptotic Bcl-2 family proteins.