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学科主题基础医学
Low Molecular Weight Fucoidan against Renal Ischemia-Reperfusion Injury via Inhibition of the MAPK Signaling Pathway
Chen, Jihui1,2; Wang, Weiling1,2; Zhang, Quanbin3; Li, Fei1,2; Lei, Tianluo1,2; Luo, Dali4; Zhou, Hong1,2; Yang, Baoxue1,2
刊名PLOS ONE
2013-02-13
DOI10.1371/journal.pone.0056224
8期:2
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
资助者National Natural Science Foundation of China ; Drug Discovery Program grant ; Doctoral Training Fund ; International Science and Technology Cooperation Program of China ; Beijing Natural Science Foundation grant ; 111 Project ; National Natural Science Foundation of China ; Drug Discovery Program grant ; Doctoral Training Fund ; International Science and Technology Cooperation Program of China ; Beijing Natural Science Foundation grant ; 111 Project
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]UNDARIA-PINNATIFIDA ; MYOCARDIAL-ISCHEMIA ; PC12 CELLS ; LAMINARIA-JAPONICA ; FREE-RADICALS ; IN-VIVO ; APOPTOSIS ; ACTIVATION ; RAT ; JNK
英文摘要

Background: Ischemia reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI) in both native and transplanted kidneys. The objective of the present study was to evaluate whether low-molecular-weight fucoidan (LMWF) could attenuate renal IRI in an animal model and in vitro cell models and study the mechanisms in which LMWF protected from IRI.

Methodology/Principal Findings: Male mice were subjected to right renal ischemia for 30 min and reperfusion for 24 h, or to a sham operation with left kidney removed. Kidneys undergone IR showed characteristic morphological changes, such as tubular dilatation, and brush border loss. However, LMWF significantly corrected the renal dysfunction and the abnormal levels of MPO, MDA and SOD induced by IR. LMWF also inhibited the activation of MAPK pathways, which consequently resulted in a significant decrease in the release of cytochrome c from mitochondria, ratios of Bax/Bcl-2 and cleaved caspase3/ caspase-3, and phosphorylation of p53. LMWF alleviated hypoxia-reoxygenation or CoCl2 induced cell viability loss and Delta Psi m dissipation in HK2 renal tubular epithelial cells, which indicates LMWF may result in an inhibition of the apoptosis pathway through reducing activity of MAPK pathways in a dose-dependent manner.

Conclusions/Significance: Our in vivo and in vitro studies show that LMWF ameliorates acute renal IRI via inhibiting MAPK signaling pathways. The data provide evidence that LMWF may serve as a potential therapeutic agent for acute renal IRI.

语种英语
所属项目编号30870921 ; 31200869 ; 81170632 ; 81261160507 ; 2009ZX09301-010-30 ; 20100001110047 ; 2012DFA11070 ; 7102105
资助者National Natural Science Foundation of China ; Drug Discovery Program grant ; Doctoral Training Fund ; International Science and Technology Cooperation Program of China ; Beijing Natural Science Foundation grant ; 111 Project ; National Natural Science Foundation of China ; Drug Discovery Program grant ; Doctoral Training Fund ; International Science and Technology Cooperation Program of China ; Beijing Natural Science Foundation grant ; 111 Project
WOS记录号WOS:000315970300131
引用统计
被引频次:25[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/400002259/52879
专题基础医学院_药理学系
作者单位1.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing, Peoples R China
2.Chinese Acad Sci, Inst Oceanol, Qingdao, Peoples R China
3.Capital Med Univ, Dept Pharmacol, Beijing, Peoples R China
4.Peking Univ, Sch Basic Med Sci, Dept Pharmacol, Beijing 100871, Peoples R China
推荐引用方式
GB/T 7714
Chen, Jihui,Wang, Weiling,Zhang, Quanbin,et al. Low Molecular Weight Fucoidan against Renal Ischemia-Reperfusion Injury via Inhibition of the MAPK Signaling Pathway[J]. PLOS ONE,2013,8(2).
APA Chen, Jihui.,Wang, Weiling.,Zhang, Quanbin.,Li, Fei.,Lei, Tianluo.,...&Yang, Baoxue.(2013).Low Molecular Weight Fucoidan against Renal Ischemia-Reperfusion Injury via Inhibition of the MAPK Signaling Pathway.PLOS ONE,8(2).
MLA Chen, Jihui,et al."Low Molecular Weight Fucoidan against Renal Ischemia-Reperfusion Injury via Inhibition of the MAPK Signaling Pathway".PLOS ONE 8.2(2013).
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