Exhaustive Exercise Increases Inflammatory Response via Toll Like Receptor-4 and NF-kappa Bp65 Pathway in Rat Adipose Tissue
Data
2011-06-01
Autores
Rosa Neto, José Cesar 
Lira, Fabio Santos de
Eguchi, Ricardo
Pimentel, Gustavo Duarte
Venancio, Daniel Paulino
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Cytokines (IL-6, IL-10, and TNF-alpha) are increased after exhaustive exercise in the retroperitoneal adipose tissue (RPAT) and mesenteric adipose tissue (MEAT). An exhaustive acute exercise protocol induces inflammation in adipose tissue that lasts 6 h after the exercise has ended. It is well-established that this protocol increases circulating plasma levels of non-esterified fatty acids (NEFAs) and lipopolysaccharides (LPS), compounds that are important in stimulating signaling via toll like receptor-4 (TLR-4) in different type cells. in the present study, we investigated the regulation of TLR-4 and DNA-binding of nuclear factor-kappa Bp65 (NF-kappa Bp65) in different depots of adipose tissue in rats after exhaustive exercise. Rats were killed by decapitation immediately (E0 group, n = 6), 2 (E2 group, n = 6), and 6 h (E6 group, n = 6) after the exhaustive exercise, which consisted of running on a treadmill (approximately 70% V-O2max) for 50 min and then running at an elevated rate that increased at 1 m/min, until exhaustion. the control group (C group, n = 6) was not subjected to exercise. in RPAT, TLR-4, MYD-88, and IkB alpha increased in the E2 group after exercise. MYD-88 and TRAF6 remained increased in the E6 group in comparison with the control group. DNA-binding of NF-kappa Bp65 was not altered. in MEAT, TLR-4, MYD-88, TRAF6, and DNA-binding of NF-kappa Bp65 were increased only in the E6 group. in conclusion, we have shown that increases in pro-inflammatory cytokines in adipose tissue pads after exhaustive exercise may be mediated via TLR-4 signaling, leading to increases in NF-kappa Bp65 binding to DNA in MEAT. J. Cell. Physiol. 226: 1604-1607, 2011. (C) 2010 Wiley-Liss, Inc.
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Journal of Cellular Physiology. Hoboken: Wiley-Blackwell, v. 226, n. 6, p. 1604-1607, 2011.