동의생리병리학회지 (Journal of Physiology & Pathology in Korean Medicine)

  • 제22권6호
  • /
  • Pages.1572-1578
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  • 2008
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  • 1738-7698(pISSN)
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  • 2288-2529(eISSN)
대한동의생리학회·한의병리학회 ( The Physiological Society of Korean Medicine and The Society of Pathology in Korean Medicine)
권호 표지

Anti-allergic Effect of Seungmagalgeun-tang through Suppression of NF-${\kappa}B$ and p38 Mitogen-Activated Protein Kinase Activation in the RBL-2H3 Cells

  • Lyu, Ji-Hyo (Clinical Research Center of Oriental Medicine, College of Oriental Medicine, Dongeui University) ;
  • Lyu, Sun-Ae (Department of Oriental Medicine, College of Oriental Medicine, Dongeui University) ;
  • Yoon, Hwa-Jung (Department of Oriental Medicine, College of Oriental Medicine, Dongeui University) ;
  • Ko, Woo-Shin (Department of Oriental Medicine, College of Oriental Medicine, Dongeui University)
  • 발행 : 2008.12.25
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초록

In previous report, Seungmagalgeun-tang (SGT) could exert its anti-inflammatory actions in the BV-2 microglial cells. However, study on the anti-inflammatory effect of SGT in mast cells has not been identified. Therefore, we examined on the anti-inflammatory effect of SGT on the phorbol 12-myristate 13-acetate (PMA) and calcium ionophore A23187-induced rat basophilic leukemia (RBL-2H3) cells. SGT inhibited the release of ${\beta}$-hexosaminidase and secretion and expression of pro-inflammatory cytokines such as tumor necrosis factor (TNF)-${\alpha}$ and interleukin (IL)-4 on RBL-2H3 cells, without affecting cell viability. The protein expression level of nuclear factor (NF)-${\kappa}B$ (p65) was decreased in the nucleus by SGT. In addition, SGT suppressed the degradation of inhibitory protein $I{\kappa}B-{\alpha}$ protein, the activation of p38 mitogen-activated protein kinase (MAPK), and the expressions of cyclooxygenase (COX)-2 mRNA and protein level in RBL-2H3 cells. These results suggest that SGT could be involved anti-allergic effect by control of NF-${\kappa}B$ (p65) translocation into the nucleus through inhibition of $I{\kappa}B-{\alpha}$ degradation and suppression of COX-2 expression.

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