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Panax Ginseng inhibited HIF-1a activation and inflammatory cytokine in HMC-1 cells activated by phorbol myristate acetate and A23187

  • Choi, In-Young (Department of Oriental Pharmacy, College of Pharmacy, Wonkwang University) ;
  • Jeong, Hyun-Ja (Biochip Research Center, Hoseo University) ;
  • An, Hyo-Jin (College of Oriental Medicine, Kyung Hee University) ;
  • Kang, Tae-Hee (College of Oriental Medicine, Kyung Hee University) ;
  • Zo, Chul-Won (College of Oriental Medicine, Kyung Hee University) ;
  • Song, Bong-Keun (College of Oriental Medicine, Wonkwang University) ;
  • Park, Eun-Jeong (College of Oriental Medicine, Wonkwang University) ;
  • Kim, Eun-Cheol (Department of Oral and Maxillofacial Pathology, College of Dentistry, Wonkwang University) ;
  • Um, Jae-Young (College of Oriental Medicine, Kyung Hee University) ;
  • Kim, Hyung-Min (College of Oriental Medicine, Kyung Hee University) ;
  • Hong, Seung-Heon (Department of Oriental Pharmacy, College of Pharmacy, Wonkwang University)
  • Published : 2008.12.31

Abstract

This study investigated the role of Panax ginseng (PG) on the phorbol myristate acetate (PMA) + calcium ionophore A23187-induced hypoxia-inducible factor-$1{\alpha}$ (HIF-$1{\alpha}$) activation, phosphorylation of the extracellular signal-regulated kinase (ERK), and inflammatory cytokine production from the human mast cell line, HMC-1. HIF-$1{\alpha}$ and phosphorylation of ERK were observed by Western blotting. The inflammatory cytokine production was determined by enzyme-linked immunosorbent assay. PG inhibited the PMA+A23187-induced HIF-$1{\alpha}$ expression and the subsequent production of vascular endothelial growth factor. In addition, PG suppressed PMA + A23187-induced phosphorylation of ERK. We also show that the increased cytokines interleukin (IL)-$1{\beta}$, IL-6, and tumour necrosis factor-${\alpha}$ level was significantly inhibited by treatment of PG. In the present study, we report for the first time that PG is an inhibitor of HIF-$1{\alpha}$ and cytokines on the mast cell-mediated inflammatory responses.

Keywords

References

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