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学科主题: 药学
题名:
w007B protects brain against ischemia-reperfusion injury in rats through inhibiting inflammation, apoptosis and autophagy
作者: Bu, Qixin1; Liu, Xiaoyan1; Zhu, Yuanjun1; Liu, Ye2; Wang, Yinye1
关键词: Cerebral ischemia-reperfusion ; w007B ; Therapeutic time window ; Apoptosis ; Inflammation ; Autophagy
刊名: BRAIN RESEARCH
发表日期: 2014-04-16
DOI: 10.1016/j.brainres.2014.02.034
卷: 1558, 页:100-108
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 ; CELL-DEATH ; HONOKIOL ; STROKE ; ACTIVATION ; MAGNOLOL ; MICE
英文摘要:

This study was designed to investigate the effect of w007B, a newly synthesized derivative of honokiol, on MCAO reperfusion, and its therapeutic time window and related mechanisms in rats. Neurological deficit scores, infarct size and brain water content were measured after 24 h reperfusion following 2 h ischemia. The results showed that w007B (10 and 50 mu g/kg, IV immediately after reperfusion) markedly decreased neurological deficit scores, reduced infarct size and alleviated brain water content, and then 50 mu g/kg w007B given within 3 h after reperfusion (5 h after ischemia) significantly attenuated ischemia-induced brain injury. Additionally, no sign of toxicity was observed when a single dose of 50 mg/kg w007B (1000 times of the highest effective dose, IF) was administered. To explore the underlying mechanisms, the expression level of apoptosis, inflammation and autophagy-related markers in brain tissue were detected with kits or by western blot. It was observed that w007B rapidly and significantly reduced caspase-3 activity and NO production in the injured semi-brain, and also lowered the level of the p65 subunit of NF-kappa B in the nucleus. Besides, it also reduced the expression of Beclin-1 and LC3B-II, and increased the level of p62, the autophagy-related proteins in I/R-injured hemisphere. In conclusion, w007B exerts neuroprotective effect on cerebral ischemia-reperfusion injury with wider therapeutic time window and better safety; its mechanisms may be associated with its anti-inflammation, anti-apoptosis and anti-autophagy action. These results suggest that w007B shows strong potential as a clinical neuroprotective candidate for the treatment of ischemic stroke. (C) 2014 Elsevier B.V. All rights reserved.

语种: 英语
所属项目编号: 2009zx09102-146 ; 61071002
项目资助者: Chinese National Technology Graveness Special Purpose Fund ; National Natural Science Foundation of China
WOS记录号: WOS:000335431200010
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/60086
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.Beijing Honghui New Med Technol Co Ltd, Beijing Daxing Biol Med Ind Base, Beijing 102600, Peoples R China

Recommended Citation:
Bu, Qixin,Liu, Xiaoyan,Zhu, Yuanjun,et al. w007B protects brain against ischemia-reperfusion injury in rats through inhibiting inflammation, apoptosis and autophagy[J]. BRAIN RESEARCH,2014,1558:100-108.
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