1. Both adiponectin and interleukin-10 inhibit LPS-induced activation of the NF-κB pathway in 3T3-L1 adipocytes.
- Author
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Lira FS, Rosa JC, Pimentel GD, Seelaender M, Damaso AR, Oyama LM, and do Nascimento CO
- Subjects
- 3T3-L1 Cells, Animals, Culture Media pharmacology, DNA metabolism, Interleukin-6 metabolism, Mice, Myeloid Differentiation Factor 88 metabolism, Protein Binding drug effects, TNF Receptor-Associated Factor 6 metabolism, Time Factors, Adipocytes drug effects, Adipocytes metabolism, Adiponectin pharmacology, Interleukin-10 pharmacology, Lipopolysaccharides pharmacology, NF-kappa B metabolism, Signal Transduction drug effects
- 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-κB) and leads to elevation of pro-inflammatory adipokines. However, the effects of adiponectin and IL-10 on NF-κB DNA binding activity (NF-κBp50 and NF-κBp65) 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 24h elevated IL-6 levels; activated the NF-κB pathway cascade; increased protein expression of IL-6R, TLR-4, MYD88, and TRAF6; and increased the nuclear activity of NF-κB (p50 and p65) DNA binding. Adiponectin and IL-10 inhibited the elevation of IL-6 levels and activated NF-κB (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-κB signaling pathways may be an excellent strategy for the treatment of inflammation in obese individuals., (Copyright © 2011 Elsevier Ltd. All rights reserved.)
- Published
- 2012
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