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Experimental Biology and Medicine 230:82-88 (2005)
© 2005 Society for Experimental Biology and Medicine


ORIGINAL RESEARCH ARTICLE

Anti-Allergic Effects of Artemisia iwayomogi on Mast Cell–Mediated Allergy Model

Sang-Hyun Kim*, Cheol-Hee Choi*, Sang-Yong Kim{dagger}, Jae-Soon Eun{ddagger} and Tae-Yong Shin{ddagger},1

* Research Center for Resistant Cells, College of Medicine, Chosun University, Gwangju, South Korea; {dagger} Division of Bio-Specimens and Herbarium, Korea National Arboretum, Gyeonggi, South Korea; {ddagger} College of Pharmacy, Woosuk University, Jeonbuk, South Korea

To whom requests for reprints should be addressed at 1 College of Pharmacy, Woosuk University, Jeonju, Jeonbuk, 565-701, South Korea. E-mail: tyshin{at}woosuk.ac.kr

The discovery of drugs for the treatment of allergic disease is an important subject in human health. The Artemisia iwayomogi (Compositae) (AIE) has been used as a traditional medicine in Korea and is known to have an anti-inflammatory effect. However, its specific mechanism of action is still unknown. In this report, we investigated the effect of AIE on the mast cell–mediated allergy model and studied the possible mechanism of action. AIE inhibited compound 48/80–induced systemic reactions and plasma histamine release in mice. AIE decreased immunoglobulin E (IgE)–mediated local allergic reaction, passive cutaneous anaphylaxis (PCA) reaction. AIE dose dependently attenuated histamine release from rat peritoneal mast cells activated by compound 48/80 or IgE. AIE decreased the compound 48/80–induced intracellular Ca2+. Furthermore, AIE decreased the phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore A23187-stimulated tumor necrosis factor-{alpha} and interleukin-6 gene expression and production in human mast cells. The inhibitory effect of AIE on the proinflammatory cytokine was p38 mitogen-activated protein kinase (MAPK) and nuclear factor-{kappa}B (NF-{kappa}B) dependent. AIE attenuated PMA plus A23187-induced degradation of I{kappa}B{alpha} and nuclear translocation of NF-{kappa}B and specifically blocked activation of p38 MAPK but not that of c-jun N-terminal kinase and extracellular signal-regulated kinase. Our findings provide evidence that AIE inhibits mast cell–derived immediate-type allergic reactions and involvement of intracellular Ca2+, proinflammatory cytokines, p38 MAPK, and NF-{kappa}B in these effects.

Key Words: Artemisia iwayomogi • intracellular Ca2+ • tumor necrosis factor-{alpha} • • interleukin-6 • p38 mitogen-activated protein kinase • nuclear factor-{kappa}B • mast cells




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