Modulation of acute and chronic inflammatory processes by a traditional medicine preparation GCSB-5 both in vitro and in vivo animal models

被引:56
作者
Chung, Hwa-Jin [1 ,2 ]
Lee, Hak-Sun [2 ]
Shin, Joon-Shik [3 ]
Lee, Sang-Ho [3 ]
Park, Byung-Mo [3 ]
Youn, You-Suk [3 ]
Lee, Sang Kook [1 ,2 ]
机构
[1] Seoul Natl Univ, Coll Pharm, Seoul 151742, South Korea
[2] Ewha Womans Univ, Coll Pharm, Seoul 120750, South Korea
[3] Jaseng Hosp Oriental Med, Jaseng Med Fdn, Seoul 135896, South Korea
关键词
GCSB-5; Acute and chronic inflammation; iNOS; NF-kappa B; Akt; RHEUMATOID-ARTHRITIS; KAPPA-B; ARACHIDONIC-ACID; PIVOTAL ROLE; CYCLOOXYGENASE; EXPRESSION; EDEMA; RAT; LIPOPOLYSACCHARIDE; MACROPHAGES;
D O I
10.1016/j.jep.2010.05.020
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Aim of this study: GCSB-5 is a traditional medicine preparation composed with six oriental herbs which have been widely used for the inflammatory diseases in Asia. In the present study, we have demonstrated the anti-inflammatory effects of GCSB-5 in vivo and in vitro along with its underlying mechanism of action. Methods: The acute and chronic inflammation models in animals were applied to investigate the anti-inflammatory effects of GCSB-5. To further investigate the mechanism of the anti-inflammatory activity, lipopolysaccharide (LPS)-induced murine macrophage RAW264.7 cells were also employed. Results: In in vivo animal model, oral administration of GCSB-5 significantly inhibited TPA- and carrageenan-induced acute edema and adjuvant-induced arthritis. The vascular permeability, leukocyte migration, and granuloma formation were also inhibited by GCSB-5. In accordance, GCSB-5 suppressed the LPS-induced nitric oxide (NO) production by the downregulation of mRNA and protein expressions of inducible nitric oxide synthase (iNOS). GCSB-5 also suppressed the expressions of cyclooxygenase-2 (COX-2) and inflammatory cytokines such as interleukin-1 beta and interferon-beta. The activation of NF-kappa B by LPS was also alleviated by GCSB-5, which correlated with its inhibitory effect on IkB degradation. The signaling pathway with the activation of Akt was also attenuated by the treatment by GCSB-5. Conclusions: Taken together, our results demonstrate that GCSB-5 reduces the development of acute and chronic inflammation and its anti-inflammatory property might in part be a function of the inhibition of iNOS and COX-2 expression via down-regulation of the Akt signal pathway and inhibition of NF-kappa B activation. These findings suggest that GCSB-5 might be an applicable therapeutic traditional medicine in the regulation of the inflammatory response. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:450 / 459
页数:10
相关论文
共 36 条
[1]   MODELS OF ARTHRITIS AND THE SEARCH FOR ANTI-ARTHRITIC DRUGS [J].
BILLINGHAM, MEJ .
PHARMACOLOGY & THERAPEUTICS, 1983, 21 (03) :389-428
[2]  
BRESNIHAN B, 1996, J RHEUMATOL, V26, P717
[3]   Mononuclear phagocytes and rheumatoid synovitis - Mastermind or workhorse in arthritis? [J].
Burmester, GR ;
Stuhlmuller, B ;
Keyszer, G ;
Kinne, RW .
ARTHRITIS AND RHEUMATISM, 1997, 40 (01) :5-18
[4]   MODULATION OF MOUSE EAR EDEMA BY CYCLOOXYGENASE AND LIPOXYGENASE INHIBITORS AND OTHER PHARMACOLOGICAL AGENTS [J].
CARLSON, RP ;
ONEILLDAVIS, L ;
CHANG, J ;
LEWIS, AJ .
AGENTS AND ACTIONS, 1985, 17 (02) :197-204
[5]   Nuclear factor κB:: a pivotal role in the systemic inflammatory response syndrome and new target for therapy [J].
Christman, JW ;
Lancaster, LH ;
Blackwell, TS .
INTENSIVE CARE MEDICINE, 1998, 24 (11) :1131-1138
[6]   The pivotal role of interleukin-1 in the clinical manifestations of rheumatoid arthritis [J].
Dayer, JM .
RHEUMATOLOGY, 2003, 42 :3-10
[7]  
De Nardin E, 2001, Ann Periodontol, V6, P30, DOI 10.1902/annals.2001.6.1.30
[8]  
Dunne M YV., 1990, Pathophysiology, "concepts of altered health states with contributors, P165
[9]   Chronic inflammation:: importance of NOD2 and NALP3 in interleukin-1β generation [J].
Ferrero-Miliani, L. ;
Nielsen, O. H. ;
Andersen, P. S. ;
Girardin, S. E. .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2007, 147 (02) :227-235
[10]   Molecular mechanisms of macrophage activation and deactivation by lipopolysaccharide: roles of the receptor complex [J].
Fujihara, M ;
Muroi, M ;
Tanamoto, K ;
Suzuki, T ;
Azuma, H ;
Ikeda, H .
PHARMACOLOGY & THERAPEUTICS, 2003, 100 (02) :171-194