N-(p-Coumaryol)-Tryptamine Suppresses the Activation of JNK/c-Jun Signaling Pathway in LPS-Challenged RAW264.7 Cells.
- Author:
Van Anh VO
1
;
Jae Won LEE
;
Jun Ho PARK
;
Jae Hyun KWON
;
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, Republic of Korea. wchun@kangwon.ac.kr
- Publication Type:Original Article
- Keywords:
N-(p-Coumaroyl) tryptamine;
RAW 264.7 cells;
Lipopolysaccharide;
iNOS;
COX-2;
JNK;
c-Jun
- MeSH:
Cytokines;
Dinoprostone;
Macrophages;
Nitric Oxide;
Phenol;
Phosphorylation;
Tumor Necrosis Factor-alpha
- From:Biomolecules & Therapeutics
2014;22(3):200-206
- CountryRepublic of Korea
- Language:English
-
Abstract:
N-(p-Coumaryol) tryptamine (CT), a phenolic amide, has been reported to exhibit anti-oxidant and anti-inflammatory activities. However, the underlying mechanism by which CT exerts its pharmacological properties has not been clearly demonstrated. The objective of this study is to elucidate the anti-inflammatory mechanism of CT in lipopolysaccharide (LPS)-challenged RAW264.7 macrophage cells. CT significantly inhibited LPS-induced extracellular secretion of pro-inflammatory mediators such as nitric oxide (NO) and PGE2, and protein expressions of iNOS and COX-2. In addition, CT significantly suppressed LPS-induced secretion of pro-inflammatory cytokines such as TNF-alpha and IL-1beta. To elucidate the underlying anti-inflammatory mechanism of CT, involvement of MAPK and Akt signaling pathways was examined. CT significantly attenuated LPS-induced activation of JNK/c-Jun, but not ERK and p38, in a concentration-dependent manner. Interestingly, CT appeared to suppress LPS-induced Akt phosphorylation. However, JNK inhibition, but not Akt inhibition, resulted in the suppression of LPS-induced responses, suggesting that JNK/c-Jun signaling pathway significantly contributes to LPS-induced inflammatory responses and that LPS-induced Akt phosphorylation might be a compensatory response to a stress condition. Taken together, the present study clearly demonstrates CT exerts anti-inflammatory activity through the suppression of JNK/c-Jun signaling pathway in LPS-challenged RAW264.7 macrophage cells.
