Phosphorylation of Akt Mediates Anti-Inflammatory Activity of 1-p-Coumaroyl beta-D-Glucoside Against Lipopolysaccharide-Induced Inflammation in RAW264.7 Cells
The Korean Journal of Physiology and Pharmacology
;
: 79-86, 2014.
Artigo
em Inglês
| WPRIM
| ID: wpr-727591
ABSTRACT
Hydroxycinnamic acids have been reported to possess numerous pharmacological activities such as antioxidant, anti-inflammatory, and anti-tumor properties. However, the biological activity of 1-p-coumaroyl beta-D-glucoside (CG), a glucose ester derivative of p-coumaric acid, has not been clearly examined. The objective of this study is to elucidate the anti-inflammatory action of CG in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophage cells. In the present study, CG significantly suppressed LPS-induced excessive production of pro-inflammatory mediators such as nitric oxide (NO) and PGE2 and the protein expression of iNOS and COX-2. CG also inhibited LPS-induced secretion of pro-inflammatory cytokines, IL-1beta and TNF-alpha. In addition, CG significantly suppressed LPS-induced degradation of IkappaB. To elucidate the underlying mechanism by which CG exerts its anti-inflammatory action, involvement of various signaling pathways were examined. CG exhibited significantly increased Akt phosphorylation in a concentration-dependent manner, although MAPKs such as Erk, JNK, and p38 appeared not to be involved. Furthermore, inhibition of Akt/PI3K signaling pathway with wortmannin significantly, albeit not completely, abolished CG-induced Akt phosphorylation and anti-inflammatory actions. Taken together, the present study demonstrates that Akt signaling pathway might play a major role in CG-mediated anti-inflammatory activity in LPS-stimulated RAW264.7 macrophage cells.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Fosforilação
/
Dinoprostona
/
Citocinas
/
NF-kappa B
/
Fator de Necrose Tumoral alfa
/
Ácidos Cumáricos
/
Glucose
/
Inflamação
/
Macrófagos
/
Óxido Nítrico
Idioma:
Inglês
Revista:
The Korean Journal of Physiology and Pharmacology
Ano de publicação:
2014
Tipo de documento:
Artigo
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