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学科主题: 基础医学
题名:
Low molecular weight fucoidan ameliorates diabetic nephropathy via inhibiting epithelial-mesenchymal transition and fibrotic processes
作者: Chen, Jihui1,2,3; Cui, Wentong4; Zhang, Quanbin5; Jia, Yingli1,2; Sun, Yi1,2; Weng, Lin1,2; Luo, Dali4; Zhou, Hong1,2; Yang, Baoxue1,2
关键词: Fucoidan ; diabetic nephropathy ; epithelialto-mesenchymal transition ; transforming growth factor-beta 1 ; extracellular matrix ; tubulointerstitial fibrosis
刊名: AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH
发表日期: 2015
卷: 7, 期:9, 页:1553-1563
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Oncology ; Medicine, Research & Experimental
研究领域[WOS]: Oncology ; Research & Experimental Medicine
关键词[WOS]: GROWTH-FACTOR-BETA ; TRANSCRIPTIONAL REGULATION ; RENAL FIBROSIS ; PATHWAYS ; KIDNEY ; CANCER ; SNAIL ; RATS ; FIBROGENESIS ; HOMEOSTASIS
英文摘要:

Diabetic nephropathy (DN) is one of the most serious microvascular complications of diabetes and may lead to end-stage renal disease (ESRD) and chronic renal failure. The aim of this study was to determine whether low-molecular-weight fucoidan (LMWF) can reduce harmful transforming growth factor-beta (TGF-beta)-mediated renal fibrosis in DN using in vitro and in vivo experimental models. The experimental results showed that LMWF significantly reversed TGF-beta 1-induced epithelial-mesenchymal transition and dose-dependently inhibited accumulation of extracellular matrix proteins, including connective tissue growth factor and fibronectin. It was found that LMWF significantly reduced blood urea nitrogen and blood creatinine in both type 1 and type 2 diabetic rat models. H&E, PAS and Masson′s trichrome staining of kidney tissue showed LMWF significantly reduced renal interstitial fibrosis. Treatment with LMWF significantly increased E-cadherin expression and reduced alpha-SMA, CTGF and fibronectin expression in both type 1 and type 2 diabetic models. LMWF also decreased the phosphorylation of Akt, ERK1/2, p38 and Smad3 in vitro and in vivo. These data suggest that LMWF may protect kidney from dysfunction and fibrogenesis by inhibiting TGF-beta pathway and have the potential benefit to slow down the progression of DN.

语种: 英语
所属项目编号: 81370783 ; 41376166 ; 81170632 ; 2012DFA11070 ; 2014-YY-03-04
项目资助者: National Natural Science Foundation of China ; 111 Project, International Science &amp ; Technology Cooperation Program of China ; Shanghai Pharmaceutical Association
WOS记录号: WOS:000364771500007
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/59783
Appears in Collections:基础医学院_期刊论文

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作者单位: 1.Peking Univ, Sch Basic Med Sci, Minist Educ, State Key Lab Nat & Biomimet Drugs,Key Lab Mol Ca, Beijing 100191, Peoples R China
2.Peking Univ, Sch Basic Med Sci, Dept Pharmacol, Beijing 100191, Peoples R China
3.Shanghai Jiao Tong Univ, Sch Med, Dept Pharm, Xin Hua Hosp, Shanghai 200092, Peoples R China
4.Capital Med Univ, Dept Pharmacol, Beijing 100069, Peoples R China
5.Chinese Acad Sci, Inst Oceanol, Qingdao 266071, Peoples R China

Recommended Citation:
Chen, Jihui,Cui, Wentong,Zhang, Quanbin,et al. Low molecular weight fucoidan ameliorates diabetic nephropathy via inhibiting epithelial-mesenchymal transition and fibrotic processes[J]. AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH,2015,7(9):1553-1563.
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