Phosphorylation of Akt Mediates Anti-Inflammatory Activity of 1-p-Coumaroyl beta-D-Glucoside Against Lipopolysaccharide-Induced Inflammation in RAW264.7 Cells.
10.4196/kjpp.2014.18.1.79
- Author:
Van Anh VO
1
;
Jae Won LEE
;
Ji Young KIM
;
Jun Ho PARK
;
Hee Jae LEE
;
Sung Soo KIM
;
Yong Soo KWON
;
Wanjoo CHUN
Author Information
1. Department of Pharmacology, College of Medicine, Kangwon National University, Chuncheon 200-701, Korea. wchun@kangwon.ac.kr
- Publication Type:Original Article
- Keywords:
1-p-coumaroyl beta-D-glucoside (CG);
Akt;
COX-2;
iNOS;
Lipopolysaccharide;
NF-kappaB;
RAW264.7 cells
- MeSH:
Coumaric Acids;
Cytokines;
Dinoprostone;
Glucose;
Inflammation*;
Macrophages;
NF-kappa B;
Nitric Oxide;
Phosphorylation*;
Tumor Necrosis Factor-alpha
- From:The Korean Journal of Physiology and Pharmacology
2014;18(1):79-86
- CountryRepublic of Korea
- Language:English
-
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.