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Evidence-Based Complementary and Alternative Medicine
Volume 2012, Article ID 457370, 12 pages
Research Article

Bojesodok-eum, a Herbal Prescription, Ameliorates Acute Inflammation in Association with the Inhibition of NF- B-Mediated Nitric Oxide and ProInflammatory Cytokine Production

1Department of Ophthalmology, Otolaryngology and Dermatology, College of Oriental Medicine, Daegu Haany University, Daegu 706-828, Republic of Korea
2Medical Research Center for Globalization of Herbal Formulation and College of Oriental Medicine, Daegu Haany University, Daegu 706-828, Republic of Korea
3Department of Herbal Pharmaceutical Engineering, Daegu Haany University, Kyung-San, Kyung-buk 712-715, Republic of Korea

Received 13 July 2012; Revised 27 August 2012; Accepted 27 August 2012

Academic Editor: Angelo Antonio Izzo

Copyright © 2012 Kook Ho Sohn 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.


Bojesodok-eum (BSE) is a herbal prescription consisting of Coptidis Rhizoma and Scutellariae Radix as main components. This paper investigated the effects of BSE on the induction of nitric oxide (NO), prostaglandin E2 (PGE2), and proinflammatory cytokines that are caused by lipopolysaccharide (LPS) in murine macrophage cell line and on the paw edema formation in animals. Administration of BSE (0.3 g/kg and 1 g/kg) in rats significantly inhibited carrageenan-induced paw edema formation, as did dexamethasone, an anti-inflammatory positive control drug. In cell model, treatment of BSE decreased the production of NO and PGE2 in RAW264.7 cells stimulated by LPS. BSE also inhibited the expression of iNOS and COX-2 protein as well as COX activity in a concentration-dependent manner. Consistently, BSE suppressed the ability of LPS to produce TNF- , interleukin-1 , and interleukin-6. LPS treatment induced nuclear NF- B level and I- B phosphorylation, which were inhibited subsequent treatment of BSE, suggesting its repression of LPS-inducible NF- B activation. BSE abrogated the induction of NO, PGE2, and proinflammatory cytokines, as well as iNOS and COX-2 protein expression in RAW264.7 cells stimulated by LPS as mediated with NF- B inhibition.