北京大学医学部机构知识库
Advanced  
IR@PKUHSC  > 北京大学药学院  > 期刊论文
学科主题: 药学
题名:
Protosappanin B protects PC12 cells against oxygen-glucose deprivation-induced neuronal death by maintaining mitochondrial homeostasis via induction of ubiquitin-dependent p53 protein degradation
作者: Zeng, Ke-Wu1; Liao, Li-Xi1; Zhao, Ming-Bo1; Song, Fang-Jiao; Yu, Qian2; Jiang, Yong1; Tu, Peng-Fei1
关键词: Mitochondrial dysfunction ; p53 ; Ubiquition-dependent degradation
刊名: EUROPEAN JOURNAL OF PHARMACOLOGY
发表日期: 2015-03-15
DOI: 10.1016/j.ejphar.2015.01.039
卷: 751, 页:13-23
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Pharmacology & Pharmacy
研究领域[WOS]: Pharmacology & Pharmacy
关键词[WOS]: ISCHEMIA-REPERFUSION INJURY ; OXIDATIVE STRESS ; OUTER-MEMBRANE ; SAPPAN LIGNUM ; HYPOXIA-ISCHEMIA ; BRAIN-INJURY ; STROKE ; FAMILY ; DAMAGE ; DIFFERENTIATION
英文摘要:

Protosappanin B (PTB) is a bioactive dibenzoxocin derivative isolated from Caesalpinia sappan L. Here, we investigated the neuroprotective effects and the potential mechanisms of PTB on oxygen-glucose deprivation (OGD)-injured PC12 cells. Results showed that PTB significantly increased cell viability, inhibited cell apoptosis and up-regulated the expression of growth-associated protein 43 (a marker of neural outgrowth). Moreover, our study revealed that PTB effectively maintained mitochondrial home-ostasis by up-regulation of mitochondrial membrane potential (MMP), inhibition of cytochrom c release from mitochondria and inactivation of mitochondrial caspase-9/3 apoptosis pathway. Further study showed that PTB significantly promoted cytoplasmic component degradation of p53 protein, a key negative regulator for mitochondrial function, resulting in a release of Bcl-2 from p53-Bc1-2 complex and an enhancing translocation of Bc1-2 to mitochondrial outer membrane. Finally, we found the degradation of p53 protein was induced by FIB via activation of a MDM2-dependent ubiquitination process. Taken together, our findings provided a new viewpoint of neuronal protection strategy for anoxia and ischemic injury with natural small molecular dibenzoxocin derivative by activating ubiquitin-dependent p53 protein degradation as well as increasing mitochondrial function. (C) 2015 Elsevier B.V. All rights reserved.

语种: 英语
所属项目编号: 2012ZX09301002-002-002 ; 81303253 ; 30873072
项目资助者: National Key Technology R &amp ; D Program "New Drug Innovation" of China ; Natural Science Foundation of China
WOS记录号: WOS:000350389300002
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/66462
Appears in Collections:北京大学药学院_期刊论文

Files in This Item:

There are no files associated with this item.


作者单位: 1.Peking Univ, Sch Pharmaceut Sci, State Key Lab Nat & Biomimet Drugs, Beijing 100191, Peoples R China
2.Peking Univ, Hosp 1, Res Studio Integrat Tradit & Western Med, Beijing 100034, Peoples R China

Recommended Citation:
Zeng, Ke-Wu,Liao, Li-Xi,Zhao, Ming-Bo,et al. Protosappanin B protects PC12 cells against oxygen-glucose deprivation-induced neuronal death by maintaining mitochondrial homeostasis via induction of ubiquitin-dependent p53 protein degradation[J]. EUROPEAN JOURNAL OF PHARMACOLOGY,2015,751:13-23.
Service
Recommend this item
Sava as my favorate item
Show this item's statistics
Export Endnote File
Google Scholar
Similar articles in Google Scholar
[Zeng, Ke-Wu]'s Articles
[Liao, Li-Xi]'s Articles
[Zhao, Ming-Bo]'s Articles
CSDL cross search
Similar articles in CSDL Cross Search
[Zeng, Ke-Wu]‘s Articles
[Liao, Li-Xi]‘s Articles
[Zhao, Ming-Bo]‘s Articles
Related Copyright Policies
Null
Social Bookmarking
Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit
所有评论 (0)
暂无评论
 
评注功能仅针对注册用户开放,请您登录
您对该条目有什么异议,请填写以下表单,管理员会尽快联系您。
内 容:
Email:  *
单位:
验证码:   刷新
您在IR的使用过程中有什么好的想法或者建议可以反馈给我们。
标 题:
 *
内 容:
Email:  *
验证码:   刷新

Items in IR are protected by copyright, with all rights reserved, unless otherwise indicated.

 

 

Valid XHTML 1.0!
Copyright © 2007-2017  北京大学医学部 - Feedback
Powered by CSpace