Effect of PEA on LPS inflammatory action in human adipocytes
被引:24
作者:
Hoareau, Laurence
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机构:Univ La Reunion, Fac Sci, Lab Biochim & Genet Mol, EA 2526, St Denis, France
Hoareau, Laurence
Ravanan, Palanlyandi
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机构:Univ La Reunion, Fac Sci, Lab Biochim & Genet Mol, EA 2526, St Denis, France
Ravanan, Palanlyandi
Gonthier, Marie Paule
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机构:Univ La Reunion, Fac Sci, Lab Biochim & Genet Mol, EA 2526, St Denis, France
Gonthier, Marie Paule
Delarue, Pierre
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机构:Univ La Reunion, Fac Sci, Lab Biochim & Genet Mol, EA 2526, St Denis, France
Delarue, Pierre
Goncalves, Jose
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机构:Univ La Reunion, Fac Sci, Lab Biochim & Genet Mol, EA 2526, St Denis, France
Goncalves, Jose
Cesari, Maya
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机构:Univ La Reunion, Fac Sci, Lab Biochim & Genet Mol, EA 2526, St Denis, France
Cesari, Maya
Festy, Franck
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机构:Univ La Reunion, Fac Sci, Lab Biochim & Genet Mol, EA 2526, St Denis, France
Festy, Franck
Roche, Regis
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机构:
Univ La Reunion, Fac Sci, Lab Biochim & Genet Mol, EA 2526, St Denis, FranceUniv La Reunion, Fac Sci, Lab Biochim & Genet Mol, EA 2526, St Denis, France
Roche, Regis
[1
]
机构:
[1] Univ La Reunion, Fac Sci, Lab Biochim & Genet Mol, EA 2526, St Denis, France
N-palmitoyiethanolamide;
human adipocytes;
IL-6;
lipopolysaccharide;
D O I:
10.1016/j.cyto.2006.06.005
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:
N-Palmitoylethanolamide (PEA) is an endogenous lipid secreted by human adipocytes that possesses numerous anti-inflammatory properties. Human adipose tissue can be subjected to modulation of its inflammatory state by lipopolysaccharide (LPS). Here we demonstrate that LPS increases the secretion of interleukin-6 (IL-6) by human mature adipocytes via activation of the NFKB pathway. This effect is not inhibited by PEA. Inversely, LPS strongly inhibits adipose cell leptin release, with PEA acting as a potentiator of this inhibitory effect. These actions are not linked to a reduction in leptin gene transcription. Thus, PEA does not have an anti-inflammatory role in the secretion of IL-6 via NFKB at the adipocyte level, but instead seems to act at the heart of the LPS-stimulated pathway, which, independently of NFKB, inhibits the secretion of leptin. (c) 2006 Elsevier Ltd. All rights reserved.