title: Modulation of acute and chronic inflammatory processes by a traditional medicine preparation GCSB-5 both in vitro and in vivo animal models.
abstract: OBJECTIVE
  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-1beta and interferon-beta. The activation of NF-kappaB 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-kappaB activation. These findings suggest that GCSB-5 might be an applicable therapeutic traditional medicine in the regulation of the inflammatory response.
authors.affiliation: College of Pharmacy, Ewha Womans University, Seoul, Republic of Korea.
authors.forename: Hwa-Jin
authors.initials: HJ
authors.lastname: Chung
authors.forename: Hak-Sun
authors.initials: HS
authors.lastname: Lee
authors.forename: Joon-Shik
authors.initials: JS
authors.lastname: Shin
authors.forename: Sang-Ho
authors.initials: SH
authors.lastname: Lee
authors.forename: Byung-Mo
authors.initials: BM
authors.lastname: Park
authors.forename: You-Suk
authors.initials: YS
authors.lastname: Youn
authors.forename: Sang Kook
authors.initials: SK
authors.lastname: Lee
mesh_terms: D000208:Acute Disease; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002460:Cell Line; D002908:Chronic Disease; D051546:Cyclooxygenase 2 / Q000187:drug effects / Q000235:genetics; D004195:Disease Models, Animal; D007249:Inflammation / Q000188:drug therapy* / Q000503:physiopathology; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008518:Medicine, East Asian Traditional; D051379:Mice; D008813:Mice, Inbred ICR; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D052247:Nitric Oxide Synthase Type II / Q000187:drug effects / Q000235:genetics; D008517:Phytotherapy / Q000379:methods; D010936:Plant Extracts / Q000494:pharmacology*; D051057:Proto-Oncogene Proteins c-akt / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000893:Anti-Inflammatory Agents; D016328:NF-kappa B; D010936:Plant Extracts; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; D051057:Proto-Oncogene Proteins c-akt