Anti-inflammatory effect of resveratrol on TNF-α-induced MCP-1 expression in adipocytes

被引：125
作者：
Zhu, Jian [1 ,2 ]
Yong, Wei [1 ]
Wu, Xiaohong [2 ]
Yu, Ying [1 ]
lv, Jinghuan [1 ]
Liu, Cuiping [2 ]
Mao, Xiaodong [2 ]
Zhu, Yunxia [1 ]
Xu, Kuanfeng [2 ]
Han, Xiao [1 ]
Liu, Chao [2 ]
机构：
[1] Nanjing Med Univ, Jiangsu Province Diabet Ctr, Sch Basic Med Sci, Key Lab Human Funct Genom Jiangsu Province, Nanjing 210029, Peoples R China
[2] Nanjing Med Univ, Dept Endocrinol, Affiliated Hosp 1, Nanjing 210029, Peoples R China
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2008年 / 369卷 / 02期
关键词：
resveratrol; NF-kappa B; MCP-1; Sirt1; 3T3-L1; adipoctye; inflammation;
D O I：
10.1016/j.bbrc.2008.02.034
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Chronic low-grade inflammation characterized by adipose tissue macrophage accumulation and abnormal cytokine production is a key feature of obesity and type 2 diabetes. Adipose-tissue-derived monocyte chemoattractant protein (MCP)-1, induced by cytokines, has been shown to play an essential role in the early events during macrophage infiltration into adipose tissue. In this study we investigated the effects of resveratrol upon both tumor necrosis factor (TNF)-alpha-induced MCP-1 gene expression and its underlying signaling pathways in 3T3-L1 adipoctyes. Resveratrol was found to inhibit TNF-alpha-induced MCP-1 secretion and gene transcription as well as promoter activity, which based on down-regulation of TNF-alpha-induced MCP-1 transcription. Nuclear factor (NF)-kappa B was determined to play a major role in the TNF-alpha-induced MCP-1 expression. Further analysis showed that resveratrol inhibited DNA binding activity of the NF-kappa B complex and subsequently suppressed NF-kappa B transcriptional activity in TNF-alpha-stimulated cells. Finally, the inhibition of MCP-1 may represent a novel mechanism of resveratrol in preventing obesity-related pathologies. (C) 2008 Elsevier Inc. All rights reserved.
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收藏
页码：471 / 477
页数：7
相关论文
共 25 条
[1]   Increased nuclear NAD biosynthesis and SIRT1 activation prevent axonal degeneration [J].
Araki, T ;
Sasaki, Y ;
Milbrandt, J .
SCIENCE, 2004, 305 (5686) :1010-1013
[2]   Mechanism of human SIRT1 activation by resveratrol [J].
Borra, MT ;
Smith, BC ;
Denu, JM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (17) :17187-17195
[3]   High-fat diet induces increased tissue expression of TNF-α [J].
Borst, SE ;
Conover, CF .
LIFE SCIENCES, 2005, 77 (17) :2156-2165
[4]   Resveratrol attenuates TNF-α-induced activation of coronary arterial endothelial cells:: role of NF-kB inhibition [J].
Csiszar, Anna ;
Smith, Kira ;
Labinskyy, Nazar ;
Orosz, Zsuzsanna ;
Rivera, Aracelie ;
Ungvari, Zoltan .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2006, 291 (04) :H1694-H1699
[5]   Macrophage TNF-α contributes to insulin resistance and hepatic steatosis in diet-induced obesity [J].
De Taeye, Bart M. ;
Novitskaya, Tatiana ;
McGuinness, Owen P. ;
Gleaves, Linda ;
Medda, Mousumi ;
Covington, Joseph W. ;
Vaughan, Douglas E. .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2007, 293 (03) :E713-E725
[6]   Monocyte chemoattractant protein 1 expression is stimulated by growth hormone and interleukin-6 in 3T3-L1 adipocytes [J].
Fasshauer, M ;
Klein, J ;
Kralisch, S ;
Klier, M ;
Lossner, U ;
Bluher, M ;
Paschke, R .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2004, 317 (02) :598-604
[7]   Chemokines control fat accumulation and leptin secretion by cultured human adipocytes [J].
Gerhardt, CC ;
Romero, IA ;
Cancello, R ;
Camoin, L ;
Strosberg, AD .
MOLECULAR AND CELLULAR ENDOCRINOLOGY, 2001, 175 (1-2) :81-92
[8]   Inflammation and metabolic disorders [J].
Hotamisligil, Goekhan S. .
NATURE, 2006, 444 (7121) :860-867
[9]   Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespan [J].
Howitz, KT ;
Bitterman, KJ ;
Cohen, HY ;
Lamming, DW ;
Lavu, S ;
Wood, JG ;
Zipkin, RE ;
Chung, P ;
Kisielewski, A ;
Zhang, LL ;
Scherer, B ;
Sinclair, DA .
NATURE, 2003, 425 (6954) :191-196
[10]  
Jain RG, 1999, J CELL PHYSIOL, V179, P58, DOI 10.1002/(SICI)1097-4652(199904)179:1<58::AID-JCP8>3.0.CO
123