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Neuroprotection against ischemic brain injury by SP600125 via suppressing the extrinsic and intrinsic pathways of apoptosis
文献类型：期刊论文
| 作者 | Guan, Qiu-Hua ; Pei, Dong-Sheng ; Liu, Xiao-Mei ; Wang, Xiao-Tian ; Xu, Tian-Le(徐天乐) ; Zhang, Guang-Yi |
| 刊名 | BRAIN RESEARCH
 |
| 出版日期 | 2006 |
| 卷号 | 1092期号:pt 1页码:36-46 |
| ISSN号 | 0006-8993 |
| 关键词 | c-Jun N-terminal protein kinase (JNK) cerebral ischemia/reperfusion extrinsic and intrinsic pathways of apoptosis SP600125 N-TERMINAL KINASE BAX-DEPENDENT APOPTOSIS FAS LIGAND NEURONAL APOPTOSIS CEREBRAL-ISCHEMIA SIGNALING PATHWAY HIPPOCAMPAL CA1 JNK DEATH PHOSPHORYLATION |
| 通讯作者 | Zhang, GY (reprint author), Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, 84 W Huai Hai Rd, Xuzhou 221002, Jiangsu, Peoples R China,gyzhang@xzmc.edu.cn |
| 英文摘要 | Our previous studies and the others have strongly suggested that JNK signaling pathway plays a critical role in ischemic brain injury. Here, we reported that SP600125, a potent, cell-permeable, selective, and reversible inhibitor of c-Jun N-terminal kinase (JNK), potently decrease neuronal apoptosis induced by global ischemia/reperfusion in the vulnerable hippocampal CA1 subregion. As a result, SP600125 diminished the increased phosphorylation of c-Jun and the increased expression of FasL induced by ischemia/reperfusion in the vulnerable hippocampal CA1 subregion. At the same time, through inhibiting phosphorylation of Bcl-2 and the release of Bax from Bcl-2/Bax dimers, SP600125 attenuated Bax translocation to mitochondria and the release of cytochrome c induced by ischemia/reperfusion (I/R). Furthermore, the activation of caspase-3 induced by ischemia/reperfusion was also significantly suppressed by preinfusion of SP600125. Importantly, the same neuropotective effect was showed by administration of SP600125 both before and after ischemia. Thus, our findings imply that SP600125 can inhibit the activation of JNK signaling pathway and induce neuroprotection against ischemia/reperfusion in rat hippocampal CA1 region via suppressing the extrinsic and intrinsic pathways of apoptosis. Taken together, these results indicate that targeting the JNK pathway provides a promising therapeutic approach for ischemic brain injury. (c) 2006 Elsevier B.V. All rights reserved. |
| 学科主题 | Neurosciences & Neurology |
| 收录类别 | SCI |
| 语种 | 英语 |
| 公开日期 | 2012-07-23 |
| 源URL | [http://ir.sibs.ac.cn/handle/331001/1819]  |
| 专题 | 上海神经科学研究所_神经所(总) |
| 推荐引用方式 GB/T 7714 | Guan, Qiu-Hua,Pei, Dong-Sheng,Liu, Xiao-Mei,et al. Neuroprotection against ischemic brain injury by SP600125 via suppressing the extrinsic and intrinsic pathways of apoptosis[J]. BRAIN RESEARCH,2006,1092(pt 1):36-46. |
| APA | Guan, Qiu-Hua,Pei, Dong-Sheng,Liu, Xiao-Mei,Wang, Xiao-Tian,Xu, Tian-Le,&Zhang, Guang-Yi.(2006).Neuroprotection against ischemic brain injury by SP600125 via suppressing the extrinsic and intrinsic pathways of apoptosis.BRAIN RESEARCH,1092(pt 1),36-46. |
| MLA | Guan, Qiu-Hua,et al."Neuroprotection against ischemic brain injury by SP600125 via suppressing the extrinsic and intrinsic pathways of apoptosis".BRAIN RESEARCH 1092.pt 1(2006):36-46. |
入库方式： OAI收割
来源：上海神经科学研究所
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