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

Author:

Kim Sang-Hyun1,Choi Cheol-Hee1,Kim Sang-Yong2,Eun Jae-Soon3,Shin Tae-Yong3

Affiliation:

1. Research Center for Resistant Cells, College of Medicine, Chosun University, Gwangju, South Korea

2. Division of Bio-Specimens and Herbarium, Korea National Arboretum, Gyeonggi, South Korea

3. College of Pharmacy, Woosuk University, J eonbuk, South Korea

Abstract

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 (lgE)–mediated local allergic reaction, passive cutaneous anaphylaxis (PCA) reaction. AIE dose dependency 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 lonophore A23187-stimulated tumor necrosis factor-α 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-κB (NF-κB) dependent. AIE attenuated PMA plus A23187-lnduced degradation of licBa and nuclear translocation of NF-κB 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-κB in these effects.

Publisher

SAGE Publications

Subject

General Biochemistry, Genetics and Molecular Biology

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