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Carabrol suppresses LPS-induced nitric oxide synthase expression by inactivation of p38 and JNK via inhibition of I-kappa B alpha degradation in RAW 264.7 cells

Authors
Lee, Hwa JinLim, Hyo JinLee, Da YeonJung, HyeyounKim, Mi-RanMoon, Dong-CheulKim, Keun IlLee, Myeong-SokRyu, Jae-Ha
Issue Date
Jan-2010
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Keywords
Carabrol; Nitric oxide; Prostaglandin E-2; Carpesium macrocephalum; Nuclear factor-kappa B
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.391, no.3, pp.1400 - 1404
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume
391
Number
3
Start Page
1400
End Page
1404
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/13291
DOI
10.1016/j.bbrc.2009.12.073
ISSN
0006-291X
Abstract
Carabrol, isolated from Carpesium macrocephalum, showed anti-inflammatory potential in LPS-induced RAW 264.7 murine macrophages. In present study, carabrol demonstrated the inhibitory activity on pro-inflammatory cytokines such as IL-1 beta, IL-6 and TNF-alpha. In addition, mRNA and protein levels of iNOS and COX-2 were reduced by carabrol. Molecular analysis revealed that these suppressive effects were correlated with the inactivation of p38 and JNK via inhibition of NF-kappa B activation. Immunoblotting showed that carabrol suppressed LPS-induced degradation of I-kappa B alpha and decreased nuclear translocation of p65. Taken together, these results suggest that carabrol can be a modulator of pro-inflammatory signal transduction pathway in RAW 264.7 cells. (C) 2009 Elsevier Inc. All rights reserved.
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이과대학 (생명시스템학부)
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