Huperzine a attenuates mitochondrial dysfunction in beta-amyloid-treated PC12 cells by reducing oxygen free radicals accumulation and improving mitochondrial energy metabolism
文献类型：期刊论文
| 作者 | Gao, X; Tang, XC
|
| 刊名 | JOURNAL OF NEUROSCIENCE RESEARCH
 |
| 出版日期 | 2006-05-01 |
| 卷号 | 83期号:6页码:1048-1057 |
| 关键词 | alzheimer's disease beta-amyloid peptide huperzine A mitochondria reactive oxygen species |
| ISSN号 | 0360-4012 |
| DOI | 10.1002/jnr.20791 |
| 文献子类 | Article |
| 英文摘要 | We observed previously that huperzine A (HupA), a selective acetylcholinesterase inhibitor, can counteract neuronal apoptosis and cell damage induced by several neurotoxic substances, and that this neuroprotective action somehow involves the mitochondria. We investigated the ability of HupA to reduce mitochondrial dysfunction in neuron-like rat pheochromocytoma (PC12) cells exposed in culture to the amyloid beta-peptide fragment 25-35 (A beta(25-35)). After exposure to 1 mu M A beta(25-35) for various periods, cells exhibited a rapid decline of ATP levels and obvious disruption of mitochondrial membrane homeostasis and integrity as determined by characteristic morphologic alterations, reduced membrane potential, and decreased activity of ion transport proteins. In addition, A beta(25-35) treatment also led to inhibition of key enzyme activities in the electron transport chain and the tricarboxylic acid cycle, as well as an increase of intracellular reactive oxygen species (ROS). Pre-incubation with HupA for 2 hr not only attenuated these signs of cellular stress caused by A beta, but also enhanced ATP concentration and decreased ROS accumulation in unharmed normal cells. Those results indicate that HupA protects mitochondria against A beta-induced damages, at least in part by inhibiting oxidative stress and improving energy metabolism, and that these protective effects reduce the apoptosis of neuronal cells exposed to this toxic peptide. (c) 2006 Wiley-Liss, Inc. |
| WOS关键词 | KETOGLUTARATE-DEHYDROGENASE COMPLEX ; RAT PHEOCHROMOCYTOMA CELLS ; K+-ATPASE ACTIVITY ; ALZHEIMERS-DISEASE ; OXIDATIVE STRESS ; CHOLINESTERASE INHIBITOR ; PYRUVATE-DEHYDROGENASE ; CORTICAL-NEURONS ; PRIMARY TARGET ; A-BETA |
| WOS研究方向 | Neurosciences & Neurology |
| 语种 | 英语 |
| WOS记录号 | WOS:000237217100012 |
| 出版者 | WILEY-LISS |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/273611]  |
| 专题 | 院士及顾问专家 中科院受体结构与功能重点实验室 新药研究国家重点实验室 |
| 通讯作者 | Tang, XC |
| 作者单位 | Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Shanghai 201203, Peoples R China |
| 推荐引用方式 GB/T 7714 | Gao, X,Tang, XC. Huperzine a attenuates mitochondrial dysfunction in beta-amyloid-treated PC12 cells by reducing oxygen free radicals accumulation and improving mitochondrial energy metabolism[J]. JOURNAL OF NEUROSCIENCE RESEARCH,2006,83(6):1048-1057. |
| APA | Gao, X,&Tang, XC.(2006).Huperzine a attenuates mitochondrial dysfunction in beta-amyloid-treated PC12 cells by reducing oxygen free radicals accumulation and improving mitochondrial energy metabolism.JOURNAL OF NEUROSCIENCE RESEARCH,83(6),1048-1057. |
| MLA | Gao, X,et al."Huperzine a attenuates mitochondrial dysfunction in beta-amyloid-treated PC12 cells by reducing oxygen free radicals accumulation and improving mitochondrial energy metabolism".JOURNAL OF NEUROSCIENCE RESEARCH 83.6(2006):1048-1057. |
入库方式： OAI收割
来源：上海药物研究所
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