Glycine suppresses TNF-alpha-induced activation of NF-kappa B in differentiated 3T3-L1 adipocytes

作者：Blancas Flores Gerardo^*; Alarcon Aguilar Francisco J; Garcia Macedo Rebeca; Almanza Perez Julio C; Flores Saenz Jose L; Roman Ramos Ruben; Ventura Gallegos Jose L; Kumate Jesus; Zentella Dehesa Alejandro; Cruz Miguel

来源：European Journal of Pharmacology, 2012, 689(1-3): 270-277.

DOI：10.1016/j.ejphar.2012.06.025

• Glycine
• Cytokines
• Inflammatory process
• NF-kappa B
• I kappa Bs

Glycine strongly reduces the serum levels of pro-inflammatory cytokines and increases the levels of anti-inflammatory cytokines. Recently, glycine has been shown to decrease the expression and secretion of pro-inflammatory adipokines in monosodium glutamate-induced obese (MSG/Ob) mice. It has been postulated that these effects may be explained by a reduction in nuclear factor kappa B (NF-kappa B) activation. NF-kappa B is a transcription factor, which is crucial to the inflammatory response. Hasegawa et al. (2011 and 2012) recently reported a glycine-dependent reduction in NF-kappa B levels. Here, we have investigated the role of glycine in the regulation of NF-kappa B in differentiated 3T3-L1 adipocytes. The results revealed that pretreatment with glycine interfered with the activation of NF-kappa B, which has been shown to be stimulated by tumor necrosis factor-alpha (TNF-alpha). Glycine alone stimulated NF-kappa B activation in an unusual way such that the inhibitor kappa B-beta (I kappa B-beta) degradation was more significant than that of the inhibitor kappa B-alpha (I kappa B-alpha) and led to NF-kappa B complexes comprised of p50 and p65 subunits; I kappa B-epsilon degradation did not affect by glycine. These findings suggest that glycine could be used as an alternative treatment for chronic inflammation, which is a hallmark of obesity and other comorbidities, and is characterized by an elevated production of pro-inflammatory cytokines.

• 出版日期2012-8-15