Study on the Anti-inflammatory Effect of Jakyak-tang Water Extract

작약탕(芍藥湯) 물 추출물의 항염증작용에 관한 연구

  • Seo, Yun-Hee (Department of Preventive Medicine, College of Oriental Medicine, Wonkwang University) ;
  • Kang, Ok-Hwa (Department of Oriental Pharmacy, College of Pharmacy, Wonkwang University) ;
  • Kwon, Dong-Yeul (Department of Oriental Pharmacy, College of Pharmacy, Wonkwang University) ;
  • Lee, Jang-Suk (Department of Preventive Medicine, College of Oriental Medicine, Wonkwang University) ;
  • Han, Jong-Hyun (Department of Pharmacology, College of Oriental Medicine, Wonkwang University) ;
  • Lee, Ki-Nam (Department of Preventive Medicine, College of Oriental Medicine, Wonkwang University) ;
  • Chong, Myong-Soo (Department of Preventive Medicine, College of Oriental Medicine, Wonkwang University)
  • 서윤희 (원광대학교 한의과대학 예방의학교실) ;
  • 강옥화 (원광대학교 약학대학 한약학과) ;
  • 권동렬 (원광대학교 약학대학 한약학과) ;
  • 이장석 (원광대학교 한의과대학 예방의학교실) ;
  • 한종현 (원광대학교 한의과대학 약리학교실) ;
  • 이기남 (원광대학교 한의과대학 예방의학교실) ;
  • 정명수 (원광대학교 한의과대학 예방의학교실)
  • Received : 2011.03.25
  • Accepted : 2011.05.04
  • Published : 2011.06.25

Abstract

Jakyaktang(芍藥湯; JYT) exhibits potent anti-inflammatory activity in widely intestinal disease, but its mechanism was undisclosed. To elucidate the molecular mechanisms of JYT on pharmacological and biochemical actions in inflammation, we examined the effect of JYT on pro-inflammatory mediators in phorbol 12-myristate 13-acetate (PMA) plus A23187-induced mast cell and lipopolysaccharide (LPS)-stimulated macrophages. The investigation focused on whether JYT inhibited pro-inflammatory cytokines such as interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) in PMA plus A23187- induced HMC-1 cells and inflammatory madiators such as nitric oxide (NO), TNF-${\alpha}$, IL-6, iNOS, COX-2 in LPS-stimulated RAW 264.7 cells. We found that JYT inhibited LPS-induced NO, TNF-${\alpha}$ and IL-6 productions as well as the expressions of iNOS and COX-2. These results suggest that JYT has inhibitory effects on mast cell-mediated and macropage-mediated inflammation.

Keywords

References

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