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  • 标题:Anti-inflammatory Effect of Columbianetin on Activated Human Mast Cells
  • 本地全文:下载
  • 作者:Hyun-Ja Jeong ; Ho-Jeong Na ; Su-Jin Kim
  • 期刊名称:Biological and Pharmaceutical Bulletin
  • 印刷版ISSN:0918-6158
  • 电子版ISSN:1347-5215
  • 出版年度:2009
  • 卷号:32
  • 期号:6
  • 页码:1027-1031
  • DOI:10.1248/bpb.32.1027
  • 出版社:The Pharmaceutical Society of Japan
  • 摘要:In the present study, we extracted Corydalis heterocarpa with various solvents in order to find the bioactive constituents that demonstrated anti-inflammatory effects. We isolated the active compound, Columbianetin. Anti-inflammatory effect of Columbianetin has been reported but the precise effects of Columbianetin in experimental models have remained unknown. In the present study, we investigate the effect of Columbianetin on the production of histamine, interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α and expression of cyclooxygenase-2 (COX-2) by using the human mast cell line (HMC-1). Various concentrations of Columbianetin were treated before the activation of HMC-1 cells with phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore, A23187. PMA plus A23187 significantly increased IL-1β, IL-6, IL-8, and TNF-α production compared with media control ( p <0.05). We also show that the increased cytokines IL-1β, IL-6, IL-8, and TNF-α level was significantly inhibited by Columbianetin in a dose-dependent manner ( p <0.05). Maximal inhibition rates of IL-1β, IL-6, IL-8, and TNF-α production by Columbianetin were about 102.6%, 101.1%, 95.8%, and 103.9%, respectively. Columbianetin inhibited expression of COX-2. In addition, the effect of Columbianetin was investigated on the histamine release from HMC-1 stimulated by substance P, which promotes histamine release. Columbianetin also inhibited the histamine release by substance P. In conclusion, these results indicate that Columbianetin may be helpful in regulating mast cell-mediated allergic inflammatory responses.
  • 关键词:Columbianetin;inflammation;mast cell;interleukin;tumor necrosis factor-α
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