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Title: Both adiponectin and interleukin-10 inhibit LPS-induced activation of the NF-kappa B pathway in 3T3-L1 adipocytes
Authors: Lira, Fábio Santos de [UNIFESP]
Rosa Neto, José Cesar [UNIFESP]
Pimentel, Gustavo Duarte [UNIFESP]
Seelaender, Marilia
Damaso, Ana Raimunda [UNIFESP]
Oyama, Lila Missae [UNIFESP]
Nascimento, Claudia Maria da Penha Oller do [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Keywords: Adiponectin
Interleukin 10
NF-kappa B pathway
Issue Date: 1-Jan-2012
Publisher: Elsevier B.V.
Citation: Cytokine. London: Academic Press Ltd- Elsevier B.V., v. 57, n. 1, p. 98-106, 2012.
Abstract: Adiponectin and interleukin 10 (IL-10) are adipokines that are predominantly secreted by differentiated adipocytes and are involved in energy homeostasis, insulin sensitivity, and the anti-inflammatory response. These two adipokines are reduced in obese subjects, which favors increased activation of nuclear factor kappa B (NF-kappa B) and leads to elevation of pro-inflammatory adipokines. However, the effects of adiponectin and IL-10 on NF-kappa B DNA binding activity (NF-kappa Bp50 and NF-kappa Bp65) and proteins involved with the toll-like receptor (TLR-2 and TLR-4) pathway, such as MYD88 and TRAF6 expression, in lipopolysaccharide-treated 3T3-L1 adipocytes are unknown. Stimulation of lipopolysaccharide-treated 3T3-L1 adipocytes for 24 h elevated IL-6 levels; activated the NF-kappa B pathway cascade; increased protein expression of IL-6R, TLR-4, MYD88, and TRAF6; and increased the nuclear activity of NF-kappa B (p50 and p65) DNA binding. Adiponectin and IL-10 inhibited the elevation of IL-6 levels and activated NF-kappa B (p50 and p65) DNA binding. Taken together, the present results provide evidence that adiponectin and IL-10 have an important role in the anti-inflammatory response in adipocytes. in addition, inhibition of NF-kappa B signaling pathways may be an excellent strategy for the treatment of inflammation in obese individuals. (C) 2011 Elsevier B.V. All rights reserved.
ISSN: 1043-4666
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