Both adiponectin and interleukin-10 inhibit LPS-induced activation of the NF-kappa B pathway in 3T3-L1 adipocytes

Author(s)

Lira, Fabio Santos ^[1] ; Rosa, Jose Cesar ^[1] ; Pimentel, Gustavo Duarte ^[1] ; Seelaender, Marilia ^[2] ; Damaso, Ana Raimunda ^[1] ; Oyama, Lila Missae ^[1] ; do Nascimento, Claudia Oller ^[1]

Affiliation

^[1] Univ Fed Sao Paulo, Dept Fis, BR-04023060 Sao Paulo - Brazil

^[2] Univ Sao Paulo, Inst Biomed Sci, Canc & Metab Grp, Sao Paulo - Brazil

• Document type: Journal article
• Source: CYTOKINE; v. 57, n. 1, p. 98-106, JAN 2012.
• Web of Science Citations: 46

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 Ltd. All rights reserved. (AU)