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Title: 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

Journal Article · · Biochemical and Biophysical Research Communications
 [1]; ;  [2];  [1]; ;  [3]; ;  [1];  [2]
  1. Department of Life Science, Research Center for Women's Diseases, Sookmyung Women's University, Seoul 140-742 (Korea, Republic of)
  2. College of Pharmacy, Sookmyung Women's University, Seoul 140-742 (Korea, Republic of)
  3. College of Pharmacy, Chungbuk National University, Cheungju 361-763 (Korea, Republic of)

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.

OSTI ID:
22202329
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 391, Issue 3; Other Information: Copyright (c) 2009 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English