Baifuzi reduces transient ischemic brain damage through an interaction with the strex domain of bkca channels
文献类型：期刊论文
| 作者 | Chi, S.1,3; Cai, W.2; Liu, P.3,6; Zhang, Z.2; Chen, X.4; Gao, L.5; Qi, J.5; Bi, L.4; Chen, L.2; Qi, Z.1,3 |
| 刊名 | Cell death & disease
 |
| 出版日期 | 2010 |
| 卷号 | 1页码:11 |
| 关键词 | Baifuzi Bkca channel Brain ischemia Cerebroside Traditional chinese medicine |
| ISSN号 | 2041-4889 |
| DOI | 10.1038/cddis.2009.10 |
| 通讯作者 | Qi, z.(qizhi@xmu.edu.cn) |
| 英文摘要 | Stroke is a long-term disability and one of the leading causes of death. however, no successful therapeutic intervention is available for the majority of stroke patients. in this study, we explored a traditional chinese medicine baifuzi (typhonium giganteum engl.). we show, at first, that the ethanol extract of baifuzi exerts neuroprotective effects against brain damage induced by transient global or focal cerebral ischemia in rats and mice. second, the extract activated large-conductance ca2+-activated k+ channel (bkca) channels, and bkca channel blockade suppressed the neuroprotection of the extract, suggesting that the bkca is the molecular target of baifuzi. third, baifuzi cerebroside (baifuzi-cb), purified from its ethanol extract, activated bkca channels in a manner similar to that of the extract. fourth, the stress axis hormone-regulated exon (strex) domain of the bkca channel directly interacted with baifuzi-cb, and its deletion suppressed channel activation by baifuzi-cb. these results indicate that baifuzi-cb activated the bkca channel through its direct interaction with the strex domain of the channel and suggests that baifuzi-cb merits exploration as a potential therapeutic agent for treating brain ischemia. cell death and disease (2010) 1, e13; doi:10.1038/cddis.2009.10; published online 21 january 2010 |
| WOS关键词 | CA2+-ACTIVATED K+ CHANNELS ; CEREBRAL-ARTERY OCCLUSION ; POTASSIUM CHANNELS ; HIPPOCAMPAL SLICES ; NEURONAL SURVIVAL ; LARGE-CONDUCTANCE ; NMDA RECEPTOR ; FATTY-ACIDS ; IN-VITRO ; STROKE |
| WOS研究方向 | Cell Biology |
| WOS类目 | Cell Biology |
| 语种 | 英语 |
| WOS记录号 | WOS:000279616300012 |
| 出版者 | NATURE PUBLISHING GROUP |
| URI标识 | http://www.irgrid.ac.cn/handle/1471x/2413702 |
| 专题 | 中国科学院大学 |
| 通讯作者 | Qi, Z. |
| 作者单位 | 1.Xiamen Univ, Coll Med, Dept Physiol, Xiamen 361005, Peoples R China 2.Nanjing Med Univ, Dept Physiol, Nanjing 210029, Peoples R China 3.Inst Biophys, State Key Lab Brain & Cognit Sci, Beijing, Peoples R China 4.Inst Biophys, Natl Lab Biomacromol, Beijing, Peoples R China 5.Zhejiang Univ, Coll Pharmaceut Sci, Hangzhou 310003, Zhejiang, Peoples R China 6.Chinese Acad Sci, Grad Univ, Beijing, Peoples R China |
| 推荐引用方式 GB/T 7714 | Chi, S.,Cai, W.,Liu, P.,et al. Baifuzi reduces transient ischemic brain damage through an interaction with the strex domain of bkca channels[J]. Cell death & disease,2010,1:11. |
| APA | Chi, S..,Cai, W..,Liu, P..,Zhang, Z..,Chen, X..,...&Qi, Z..(2010).Baifuzi reduces transient ischemic brain damage through an interaction with the strex domain of bkca channels.Cell death & disease,1,11. |
| MLA | Chi, S.,et al."Baifuzi reduces transient ischemic brain damage through an interaction with the strex domain of bkca channels".Cell death & disease 1(2010):11. |
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来源：中国科学院大学
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