Huperzine A and tacrine attenuate beta-amyloid peptide-induced oxidative injury
文献类型：期刊论文
| 作者 | Xiao, XQ; Wang, R; Tang, XC
|
| 刊名 | JOURNAL OF NEUROSCIENCE RESEARCH
 |
| 出版日期 | 2000-09-01 |
| 卷号 | 61期号:5页码:564-569 |
| 关键词 | Alzheimer's disease free radicals antioxidant enzymes malondialdehyde (MDA) amyloid beta-peptide |
| ISSN号 | 0360-4012 |
| 文献子类 | Article |
| 英文摘要 | Increased oxidative stress resulting from free radical damage to cellular function is associated with a number of neurodegenerative diseases, in particular with Alzheimer's disease (AD). The deposition of amyloid beta-peptide (A beta), the major pathological hallmark for AD, has been suggested as the central disease-causing and disease-promoting event for the disease, and the pathological role of A beta was partially mediated by oxidative stress. Here we compared the effects of huperzine A (HupA) and tacrine, two acetylcholinesterase (AChE) inhibitors available for AD, on A beta-induced cell lesion, level of lipid peroxidation, and antioxidant enzyme activities in rat PC12 and primary cultured cortical neurons. Following exposure of both cells to different concentrations of an active fragment of A beta, a marked reduction in cell survival and activities of glutathione peroxidase (GSH-Px) and catalase (CAT), as well as increased production of malondialdehyde (MDA) and superoxide dismutase (SOD), were observed. Pretreatment of the cells with HupA or tacrine (0.1-10 mu M) prior to A beta exposure significantly elevated the cell survival and GSH-Px and CAT activities and decreased the level of MDA. Both drugs have similar protection against A beta insult. Our results indicate that HupA and tacrine exert neuroprotective effects against A beta toxicity, which might be of importance and might contribute to their clinical efficacy for the treatment of AD. (C) 2000 Wiley-Liss, Inc. |
| WOS关键词 | SPATIAL WORKING-MEMORY ; NERVE GROWTH-FACTOR ; ALZHEIMERS-DISEASE ; HYDROGEN-PEROXIDE ; STRESS ; PROTEIN ; BRAIN ; NEUROTOXICITY ; CALCIUM ; MODEL |
| WOS研究方向 | Neurosciences & Neurology |
| 语种 | 英语 |
| WOS记录号 | WOS:000089023900011 |
| 出版者 | WILEY |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/274583]  |
| 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 200031, Peoples R China |
| 推荐引用方式 GB/T 7714 | Xiao, XQ,Wang, R,Tang, XC. Huperzine A and tacrine attenuate beta-amyloid peptide-induced oxidative injury[J]. JOURNAL OF NEUROSCIENCE RESEARCH,2000,61(5):564-569. |
| APA | Xiao, XQ,Wang, R,&Tang, XC.(2000).Huperzine A and tacrine attenuate beta-amyloid peptide-induced oxidative injury.JOURNAL OF NEUROSCIENCE RESEARCH,61(5),564-569. |
| MLA | Xiao, XQ,et al."Huperzine A and tacrine attenuate beta-amyloid peptide-induced oxidative injury".JOURNAL OF NEUROSCIENCE RESEARCH 61.5(2000):564-569. |
入库方式： OAI收割
来源：上海药物研究所
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