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ORIGINAL RESEARCH ARTICLE

Amomum xanthiodes Inhibits Mast Cell–Mediated Allergic Reactions Through the Inhibition of Histamine Release and Inflammatory Cytokine Production

Sang-Hyun Kim^* and Tae-Yong Shin^,1

^* Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu, South Korea; and 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

In this study, we investigated the effect of Amomum xanthiodes (Zingiberaceae) extract (AXE) on the mast cell–mediated allergy model and studied the possible mechanism of action. We found that AXE inhibited compound 48/80–induced systemic reactions and plasma histamine release in mice. Additionally, AXE decreased immunoglobulin E (IgE)-mediated local allergic reactions and passive cutaneous anaphylaxis (PCA), and AXE dose-dependently attenuated the release of histamine from rat peritoneal mast cells (RPMC) activated by compound 48/80 or IgE. The amounts of AXE needed for inhibition of compound 48/80–induced plasma histamine release and PCA were similar to disodium cromoglycate, the known anti-allergic drug. We found that AXE increased the cAMP levels and decreased the compound 48/80–induced intracellular Ca²⁺. Furthermore, AXE attenuated the phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore (A23187)–stimulated tumor necrosis factor- (TNF-) and interleukin (IL)-6 secretion in human mast cells. The inhibitory effect of AXE on the proinflammatory cytokines was nuclear factor-B (NF-B)–dependent. In addition, AXE decreased PMA plus A23187–induced degradation of IBand the nuclear translocation of NF-B. Our findings provide evidence that AXE inhibits mast cell–derived immediate-type allergic reactions, and that cAMP, intracellular Ca²⁺, proinflammatory cytokines, and NF-B are involved in these effects.

Key Words: Amomum xanthiodes • histamine • cAMP • intracellular Ca²⁺ • tumor necrosis factor-interleukin-6 • nuclear factor-B • mast cells

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