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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 Jin; Lim, Hyo Jin; Lee, Da Yeon; Jung, Hyeyoun; Kim, Mi-Ran; Moon, Dong-Cheul; Kim, Keun Il; Lee, Myeong-Sok; Ryu, 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
- Pages
- 5
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 391
- Number
- 3
- Start Page
- 1400
- End Page
- 1404
- ISSN
- 0006-291X
1090-2104
- 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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Related Researcher
- Kim, Keun Il
- Science (Division of Biological Sciences)