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学科主题: 药学
题名:
Honokiol protects brain against ischemia-reperfusion injury in rats through disrupting PSD95-nNOS interaction
作者: Hu, Zhenyu1; Bian, Xiling1; Liu, Xiaoyan1; Zhu, Yuanjun1; Zhang, Xiaoyi2; Chen, Shizhong3; Wang, Kewei1; Wang, Yinye1
关键词: Honokiol ; Cerebral ischemia-reperfusion ; Therapeutic time window ; PSD95-nNOS ; NMDA
刊名: BRAIN RESEARCH
发表日期: 2013-01-23
DOI: 10.1016/j.brainres.2012.11.004
卷: 1491, 页:204-212
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Neurosciences
研究领域[WOS]: Neurosciences & Neurology
关键词[WOS]: CEREBRAL-ARTERY OCCLUSION ; NMDA RECEPTOR ; IN-VIVO ; DAMAGE ; STROKE ; APOPTOSIS ; MAGNOLOL ; NNOS ; MICE ; ACTIVATION
英文摘要:

Honokiol, a major bioactive constituent of the bark of Magnolia officinalis has been confirmed to have the neuroprotective effect on ischemic stroke in rats. This study was designed to observe the therapeutic time window of honokiol microemulsion on cerebral ischemia-reperfusion injury to support its potential for future clinical trials and further explore the underlying mechanisms. Honokiol microemulsion (50 mu g/kg, i.v. at 0, 1 or 3 h after reperfusion) significantly reduced neurological deficit, infarct volume and brain water content in rats subjected to cerebral ischemia-reperfusion, and honokiol (0.1-10 mu M) significantly attenuated oxygen-glucose deprivation- or glutamate-induced injury of fetal rat cortical neurons. In co-immunoprecipitation and western blot test, honokiol decreased the intensity of nNOS related to PSD95 but failed to affect that of PSD95 related to NR2B in NR2B-PSD95-nNOS complex, and it also inhibited the translocation of nNOS from cytosol to membrane without affecting total nNOS expression, and then markedly decreased NO production in cortical neurons. Besides, the results of whole-cell patch-clamp recordings showed that honokiol reversibly inhibited the NMDA current by about 64%. In conclusion, honokiol has a therapeutic window of at least 5 h after the onset of cerebral ischemia or 3 h after reperfusion in rats, which may be in part ascribed to the disruption of the PSD95-nNOS interaction leading to the inhibition of neurotoxic NO production. (C) 2012 Elsevier B.V. All rights reserved.

语种: 英语
所属项目编号: 2009zx09102-146 ; 81000552
项目资助者: National Science and Technology Major Project ; Natural Science Foundation of China
WOS记录号: WOS:000314321600022
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内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/64117
Appears in Collections:北京大学药学院_期刊论文

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作者单位: 1.Peking Univ, Hlth Sci Ctr, Dept Mol & Cellular Pharmacol, Sch Pharmaceut Sci, Beijing 100191, Peoples R China
2.Capital Med Univ, Beijing Area Major Lab Peptide & Small Mol Drugs, Coll Pharmaceut Sci & Chem Biol, Beijing 100069, Peoples R China
3.Peking Univ, Hlth Sci Ctr, Sch Pharmaceut Sci, Dept Nat Med, Beijing 100191, Peoples R China

Recommended Citation:
Hu, Zhenyu,Bian, Xiling,Liu, Xiaoyan,et al. Honokiol protects brain against ischemia-reperfusion injury in rats through disrupting PSD95-nNOS interaction[J]. BRAIN RESEARCH,2013,1491:204-212.
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