title: Oestrogen exerts anti-inflammation via p38 MAPK/NF-κB cascade in adipocytes.
abstract: Oestrogen has anti-inflammatory property in obesity. However, the mechanism is still not defined.
  
  
  
  To investigate the effect of oestrogen on LPS-induced monocyte chemoattractant protein-1 (MCP-1) production in adipocytes.
  
  
  
  Lipopolysaccharides (LPS) was used to imitate inflammatory responses and monocyte chemotactic protein-1 (MCP-1) was selected as an inflammatory marker to observe. 17β-Estradiol (E2), SB203580 (SB), pyrrolidine dithiocarbamate (PDTC), pertussis toxin (PTX), wortmannin (WM), p65 siRNA and p38 MAPK siRNA were pre-treated respectively or together in LPS-induced MCP-1. Then p38 MAPK and NF-κB cascade were silenced successively to observe the change of each other. Lastly, oestrogen receptor (ER) α agonist, ERβ agonist and ER antagonist were utilised.
  
  
  
  LPS-induced MCP-1 largely impaired by pre-treatment with E2, SB, PDTC or silencing NF-κB subunit. E2inhibited LPS-induced MCP-1 in a time- and dose-dependent manner, which was related to the suppression of p65 translocation to nucleus. Furthermore, LPS rapidly activated p38 MAPK, while E2markedly inhibited this activation. It markedly attenuated LPS-stimulated p65 translocation to nucleus and MCP-1 production by transfecting with p38 MAPK siRNA or using p38 MAPK inhibitor. The oestrogen's inhibitory effect was mimicked by the ERα agonist, but not by the ERβ agonist. The inhibition of E2on p38 MAPK phosphorylation was prevented by ER antagonist.
  
  
  
  E2inhibits LPS-stimulated MCP-1 in adipocytes. This effect is related to the inhibition of p38 MAPK/NF-κB cascade, and ERα appears to be the dominant ER subtype in these events.
authors.affiliation: Department of Endocrinology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China.
authors.forename: Pan-Wei
authors.initials: PW
authors.lastname: Mu
authors.affiliation: Department of Physiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510630, China; Department of Physiology, School of Basic Medicine, Xinjiang Medical University, Urumqi 830011, China.
authors.forename: Ping
authors.initials: P
authors.lastname: Jiang
authors.affiliation: Department of Endocrinology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China.
authors.forename: Man-Man
authors.initials: MM
authors.lastname: Wang
authors.affiliation: Department of Endocrinology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China.
authors.forename: Yan-Ming
authors.initials: YM
authors.lastname: Chen
authors.affiliation: Department of Physiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510630, China; Research Center of Translational Medicine, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China.
authors.forename: Shu-Hui
authors.initials: SH
authors.lastname: Zheng
authors.affiliation: Department of Physiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510630, China.
authors.forename: Zhi
authors.initials: Z
authors.lastname: Tan
authors.affiliation: Department of Endocrinology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Jiang
authors.affiliation: Department of Endocrinology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China.
authors.forename: Long-Yi
authors.initials: LY
authors.lastname: Zeng
authors.affiliation: Department of Physiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510630, China. Electronic address: wangth@mail.sysu.edu.cn.
authors.forename: Ting-Huai
authors.initials: TH
authors.lastname: Wang
mesh_terms: D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism*; D000273:Adipose Tissue / Q000166:cytology / Q000378:metabolism; D000818:Animals; D001692:Biological Transport; D002467:Cell Nucleus; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000378:metabolism*; D004958:Estradiol / Q000378:metabolism* / Q000494:pharmacology; D065171:Estrogen Receptor Antagonists / Q000494:pharmacology; D047628:Estrogen Receptor alpha / Q000378:metabolism*; D004967:Estrogens / Q000378:metabolism / Q000494:pharmacology; D005260:Female; D007249:Inflammation / Q000139:chemically induced / Q000209:etiology / Q000378:metabolism*; D008070:Lipopolysaccharides; D016328:NF-kappa B / Q000378:metabolism*; D009765:Obesity / Q000150:complications / Q000378:metabolism; D010766:Phosphorylation; D011759:Pyrrolidines / Q000378:metabolism; D034741:RNA, Small Interfering / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D013859:Thiocarbamates / Q000378:metabolism; D051996:Transcription Factor RelA / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism*
chemical_list: C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D065171:Estrogen Receptor Antagonists; D047628:Estrogen Receptor alpha; D004967:Estrogens; D008070:Lipopolysaccharides; D016328:NF-kappa B; D011759:Pyrrolidines; D034741:RNA, Small Interfering; D013859:Thiocarbamates; D051996:Transcription Factor RelA; C020972:pyrrolidine dithiocarbamic acid; D004958:Estradiol; D048051:p38 Mitogen-Activated Protein Kinases
keywords: 17β-Estradiol; Adipocytes; Anti-inflammation; Monocyte chemoattractant protein-1; p38 MAPK/NF-κB