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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; Zhou, H
2013-02-13
发表期刊PLOS ONE
ISSN1932-6203
卷号8期号:2页码:e562240
文章类型Article
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.; 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.
学科领域Science & Technology - Other Topics
DOI10.1371/journal.pone.0056224
URL查看原文
收录类别SCI
语种英语
WOS研究方向Science & Technology - Other Topics
WOS类目Multidisciplinary Sciences
WOS记录号WOS:000315970300131
WOS关键词UNDARIA-PINNATIFIDA ; MYOCARDIAL-ISCHEMIA ; PC12 CELLS ; LAMINARIA-JAPONICA ; FREE-RADICALS ; IN-VIVO ; APOPTOSIS ; ACTIVATION ; RAT ; JNK
WOS标题词Science & Technology
引用统计
被引频次:53[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.qdio.ac.cn/handle/337002/16707
专题海洋生物技术研发中心
通讯作者Zhou, H
作者单位1.Peking Univ, Sch Basic Med Sci, Dept Pharmacol, Beijing 100871, Peoples R China
2.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing, Peoples R China
3.Chinese Acad Sci, Inst Oceanol, Qingdao, Peoples R China
4.Capital Med Univ, Dept Pharmacol, Beijing, Peoples R China
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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):e562240.
APA Chen, Jihui.,Wang, Weiling.,Zhang, Quanbin.,Li, Fei.,Lei, Tianluo.,...&Zhou, H.(2013).Low Molecular Weight Fucoidan against Renal Ischemia-Reperfusion Injury via Inhibition of the MAPK Signaling Pathway.PLOS ONE,8(2),e562240.
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):e562240.
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