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Cordycepin inhibits lipopolysaccharide-induced inflammation by the suppression of NF-κB through Akt and p38 inhibition in RAW 264.7 macrophage cells

Authors
 Ho Gyoung Kim  ;  Bhushan Shrestha  ;  So Yeon Lim  ;  Deok Hyo Yoon  ;  Woo Chul Chang  ;  Dong-Jik Shin  ;  Sang Kuk Han  ;  Sang Min Park  ;  Jung Hee Park  ;  Hae Il Park  ;  Jae-Mo Sung  ;  Yangsoo Jang  ;  Namsik Chung  ;  Ki-Chul Hwang  ;  Tae Woong Kim 
Citation
 EUROPEAN JOURNAL OF PHARMACOLOGY, Vol.545(2-3) : 192-199, 2006 
Journal Title
 EUROPEAN JOURNAL OF PHARMACOLOGY 
ISSN
 0014-2999 
Issue Date
2006
Keywords
Cordyceps militaris ; Cordycepin ; Macrophage ; Inflammation ; NO production ; Lipopolysaccharide (LPS)
Abstract
Cordyceps militaris, a caterpillar-grown traditional medicinal mushroom, produces an important bioactive compound, cordycepin (3'-deoxyadenosine). Cordycepin is reported to possess many pharmacological activities including immunological stimulating, anti-cancer, anti-virus and anti-infection activities. The molecular mechanisms of cordycepin on pharmacological and biochemical actions of macrophages in inflammation have not been clearly elucidated yet. In the present study, we tested the role of cordycepin on the anti-inflammation cascades in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. In LPS-activated macrophage, nitric oxide (NO) production was inhibited by butanol fraction of C. militaris and the major component of C. militaris butanol faction was identified as cordycepin by high performance liquid chromatography. To investigate the mechanism by which cordycepin inhibits NO production and inducible nitric oxide synthase (iNOS) expression, we examined the activation of Akt and MAP kinases in LPS-activated macrophage. Cordycepin markedly inhibited the phosphorylation of Akt and p38 in dose-dependent manners in LPS-activated macrophage. Moreover, cordycepin suppressed tumor necrosis factor (TNF-alpha) expression, IkappaB alpha phosphorylation, and translocation of nuclear factor-kappaB (NF-kappaB). The expressions of cycloxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were significantly decreased in RAW 264.7 cell by cordycepin. Taken together, these results suggest that cordycepin inhibits the production of NO production by down-regulation of iNOS and COX-2 gene expression via the suppression of NF-kappaB activation, Akt and p38 phosphorylation. Thus, cordycepin may provide a potential therapeutic approach for inflammation-associated disorders.
Full Text
http://www.sciencedirect.com/science/article/pii/S0014299906006674
DOI
10.1016/j.ejphar.2006.06.047
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
5. Research Institutes (연구소) > Research Center for Human Natural Defense System (생체방어연구센터) > 1. Journal Papers
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Jang, Yang Soo(장양수) ORCID logo https://orcid.org/0000-0002-2169-3112
Chung, Nam Sik(정남식)
Hwang, Ki Chul(황기철)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/108954
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