作者: Hong‐Yu Zhang , Xie Zhang , Zhou‐Guang Wang , Hong‐Xue Shi , Fen‐Zan Wu
DOI: 10.1111/CNS.12013
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摘要: Summary Aim To investigate the mechanism of endoplasmic reticulum (ER) stress–induced apoptosis as well protective action basic fibroblast growth factor (bFGF) both in vivo and vitro. Methods Results ER was involved injuries spinal cord injury (SCI) model rat. bFGF administration improved recovery increased survival neurons lesions The effect is related to inhibition CHOP, GRP78 caspase-12, which are ER response proteins. also expression growth-associated protein 43 (GAP43), neural regeneration. activation downstream signals, PI3K/Akt/GSK-3β ERK1/2, especially stress cell model. Conclusions This first study illustrate that role SCI death via signals. Our work suggested a new trend for drug development central system injuries, chronic apoptosis.