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Mediators of Inflammation
Volume 2007, Article ID 93148, 9 pages
http://dx.doi.org/10.1155/2007/93148
Research Article

Inhibitory Effect of Inflexinol on Nitric Oxide Generation and iNOS Expression via Inhibition of NF-κB Activation

Jae Woong Lee,1 Moon Soon Lee,2 Tae Hun Kim,1 Hwa Jeong Lee,1 Seong Su Hong,1 Young Hee Noh,3 Bang Yeon Hwang,1 Jai Seup Ro,1 and Jin Tae Hong1

1College of Pharmacy and CBITRC, Chungbuk National University 12, Gaesin-dong, Heungduk-gu, Cheongju, Chungbuk 361-763, South Korea
2National Institute of Environmental Research, Kyungseo-dong, Seo-gu, Incheon 404-780, South Korea
3Department of Medical Beauty, Konyang University, 26 Nae-dong, Nonsan, Chungnam 320-711, South Korea

Received 6 October 2006; Accepted 24 January 2007

Copyright © 2007 Jae Woong Lee et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Inflexinol, an ent-kaurane diterpenoid, was isolated from the leaves of Isodon excisus. Many diterpenoids isolated from the genus Isodon (Labiatae) have antitumor and antiinflammatory activities. We investigated the antiinflammatory effect of inflexinol in RAW 264.7 cells and astrocytes. As a result, we found that inflexinol (1, 5, 10 μM) suppressed the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) as well as the production of nitric oxide (NO) in LPS-stimulated RAW 264.7 cells and astrocytes. Consistent with the inhibitory effect on iNOS and COX-2 expression, inflexinol also inhibited transcriptional and DNA binding activity of NF-κB via inhibition of IκB degradation as well as p50 and p65 translocation into nucleus. These results suggest that inflexinol inhibits iNOS and COX-2 expression through inhibition of NF-κB activation, thereby inhibits generation of inflammatory mediators in RAW 264.7 cells and astrocytes, and may be useful for treatment of inflammatory diseases.