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w007B protects brain against ischemia-reperfusion injury in rats through inhibiting inflammation, apoptosis and autophagy
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
2014-04-16
DOI10.1016/j.brainres.2014.02.034
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
WOS记录号WOS:000335431200010
项目编号2009zx09102-146 ; 61071002
资助机构Chinese National Technology Graveness Special Purpose Fund ; National Natural Science Foundation of China
引用统计
被引频次:14[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/60086
专题北京大学药学院
北京大学药学院_分子与细胞药理学系
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
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GB/T 7714
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.
APA Bu, Qixin,Liu, Xiaoyan,Zhu, Yuanjun,Liu, Ye,&Wang, Yinye.(2014).w007B protects brain against ischemia-reperfusion injury in rats through inhibiting inflammation, apoptosis and autophagy.BRAIN RESEARCH,1558,100-108.
MLA Bu, Qixin,et al."w007B protects brain against ischemia-reperfusion injury in rats through inhibiting inflammation, apoptosis and autophagy".BRAIN RESEARCH 1558(2014):100-108.
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