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首页> 外文期刊>CNS neuroscience & therapeutics. >Exogenous Basic Fibroblast Growth Factor Inhibits ER Stress–Induced Apoptosis and Improves Recovery from Spinal Cord Injury
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Exogenous Basic Fibroblast Growth Factor Inhibits ER Stress–Induced Apoptosis and Improves Recovery from Spinal Cord Injury

机译：外源性碱性成纤维细胞生长因子抑制内质网应激诱导的细胞凋亡并改善脊髓损伤的恢复

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Summary Aim To investigate the mechanism of endoplasmic reticulum (ER) stress–induced apoptosis as well as the protective action of basic fibroblast growth factor ( bFGF ) both in vivo and in vitro . Methods and Results ER stress–induced apoptosis was involved in the injuries of spinal cord injury (SCI) model rat. bFGF administration improved the recovery and increased the survival of neurons in spinal cord lesions in model rat. The protective effect of bFGF is related to the inhibition of CHOP, GRP78 and caspase‐12, which are ER stress–induced apoptosis response proteins. bFGF administration also increased the survival of neurons and the expression of growth‐associated protein 43 (GAP43), which is related to neural regeneration. The protective effect of bFGF is related to the activation of downstream signals, PI3K/Akt/GSK‐3β and ERK1/2, especially in the ER stress cell model. Conclusions This is the first study to illustrate that the role of bFGF in SCI recovery is related to the inhibition of ER stress–induced cell death via the activation of downstream signals. Our work also suggested a new trend for bFGF drug development in central neural system injuries, which are involved in chronic ER stress–induced apoptosis.
机译：摘要目的探讨内质网（ER）应激诱导的细胞凋亡机制以及碱性成纤维细胞生长因子（bFGF）在体内和体外的保护作用。方法和结果ER应激诱导的细胞凋亡与脊髓损伤（SCI）模型大鼠的损伤有关。施用bFGF可改善模型大鼠脊髓损伤中神经元的恢复并提高其存活率。 bFGF的保护作用与抑制CHO应激引起的细胞凋亡反应蛋白CHOP，GRP78和caspase-12有关。施用bFGF还可以增加神经元的存活率以及与神经再生相关的生长相关蛋白43（GAP43）的表达。 bFGF的保护作用与下游信号PI3K / Akt /GSK-3β和ERK1 / 2的激活有关，特别是在ER应激细胞模型中。结论这是第一项说明bFGF在SCI恢复中的作用与通过下游信号的激活抑制ER应激引起的细胞死亡有关的研究。我们的工作还提出了中枢神经系统损伤中bFGF药物开发的新趋势，该损伤与慢性ER应激诱导的细胞凋亡有关。

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