Inhibition of Inducible Nitric Oxide Synthase and Cyclooxygenase-2 by Gamijihwang-tang Via Suppression of Nuclear Factor-B Activation in RAW 264.7 cells

Asthma is recognized today as an inflammatory disease of the lung characterized by acute non-specific airway hypersensitiveness in association with chronic pulmonary inflammation. Gamijihwang-tang(GJT), a fortified prescription of YMJHT, is applied for the treatments of chronic coughing and asthma,...

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Published in동의생리병리학회지 Vol. 19; no. 5; pp. 1405 - 1410
Main Authors Du Hyun Jang, Ji Young Kim, Eun Hee Han, Hee Ok Park, Dong Hee Kim, Hye Gwang Jeong, Dong Yeol Yoo
Format Journal Article
LanguageEnglish
Published 한의병리학회 01.10.2005
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Summary:Asthma is recognized today as an inflammatory disease of the lung characterized by acute non-specific airway hypersensitiveness in association with chronic pulmonary inflammation. Gamijihwang-tang(GJT), a fortified prescription of YMJHT, is applied for the treatments of chronic coughing and asthma, and post-delivery coughing and asthma in the gynecology. Also in the clinical practice, GJT is known to be very effective for controlling coughing and asthma as a cold sequela. In this study, we investigated the effects of GJT on the lipopolysaccharide (LPS)-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production, and on the level of inducible nitric oxide synthase (iNOS) and Cyclooxygenase-2 expression in murine macrophage RAW 264.7 cells. We found that GJT inhibited LPS-induced NO and PGE2 production in a dose dependent manner. Furthermore, GJT inhibited the expression of LPS-induced iNOS and COX-2 protein and mRNA expression in RAW 264.7 macrophages. Treatment with GJT of RAW 264.7 cells transfected with a reporter construct indicated a reduced level of LPS-induced nuclear factor-κB (NF-κB) activity and effectively lowered NF-κB binding as measured by transient transfection assay. These results suggest that the main inhibitory mechanism of the GJT may be the reduction of iNOS and COX-2 gene expression through blocking of NF-κB activation. KCI Citation Count: 0
Bibliography:G704-000534.2005.19.5.020
ISSN:1738-7698
2288-2529