Aromadendrin Inhibits Lipopolysaccharide-Induced Nuclear Translocation of NF-kappaB and Phosphorylation of JNK in RAW 264.7 Macrophage Cells.
- Author:
Jae Won LEE
1
;
Nam Ho KIM
;
Ji Young KIM
;
Jun Ho PARK
;
Seung Yeon SHIN
;
Yong Soo KWON
;
Hee Jae LEE
;
Sung Soo KIM
;
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:
Aromadendrin;
COX-2;
iNOS;
JNK;
Lipopolysaccharide;
NF-kappaB;
RAW 264.7 cells
- MeSH:
Cytoplasm;
Dinoprostone;
Macrophages*;
NF-kappa B*;
Nitric Oxide;
Phosphorylation*;
Transcription Factors
- From:Biomolecules & Therapeutics
2013;21(3):216-221
- CountryRepublic of Korea
- Language:English
-
Abstract:
Aromadendrin, a flavonol, has been reported to possess a variety of pharmacological activities such as anti-inflammatory, antioxidant, and anti-diabetic properties. However, the underlying mechanism by which aromadendrin exerts its biological activity has not been extensively demonstrated. The objective of this study is to elucidate the anti-inflammatory mechanism of aromadedrin in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. Aromadendrin significantly suppressed LPS-induced excessive production of pro-inflammatory mediators such as nitric oxide (NO) and PGE2. In accordance, aromadendrin attenuated LPS-induced overexpression iNOS and COX-2. In addition, aromadendrin significantly suppressed LPS-induced degradation of IkappaB, which sequesters NF-kappaB in cytoplasm, consequently inhibiting the nuclear translocation of pro-inflammatory transcription factor NF-kappaB. To elucidate the underlying signaling mechanism of anti-inflammatory activity of aromadendrin, MAPK signaling pathway was examined. Aromadendrin significantly attenuated LPS-induced activation of JNK, but not ERK and p38, in a concentration-dependent manner. Taken together, the present study clearly demonstrates that aromadendrin exhibits anti-inflammatory activity through the suppression of nuclear translocation of NF-kappaB and phosphorylation of JNK in LPS-stimulated RAW 264.7 macrophage cells.
