Clinopodium gracile inhibits mast cell-mediated allergic inflammation: involvement of calcium and nuclear factor-κB

Author:

Park Seung-Bin1,Kim Sang-Hyun1,Suk Kyoungho1,Lee Hyun-Shik2,Kwon Taeg Kyu3,Ju Min-Gyu4,Jeon Hoon4,Kim Dae-Keun4,Lim Jong-Pil4,Shin Tae-Yong4

Affiliation:

1. CMRI, Department of Pharmacology, School of Medicine, Kyungpook National University Medical School, Daegu 700-422

2. School of Life Sciences and Biotechnology, Kyungpook National University, Daegu 702-701

3. Department of Immunology, School of Medicine, Keimyung University, Taegu 700-712

4. College of Pharmacy, Woosuk University, Jeonju 565-701, South Korea

Abstract

Mast cell-mediated allergic disease is involved in many diseases such as anaphylaxis, rhinitis, asthma and atopic dermatitis. The discovery of drugs for the treatment of allergic disease is an important subject in human health. In this study, we investigated the effect of the water extract of Clinopodium gracile Matsum var. multicaule (WECG) on the mast cell-mediated allergic inflammation and studied the possible mechanism of action. WECG inhibited compound 48/80-induced systemic anaphylaxis and immunoglobulin E-mediated cutaneous anaphylaxis in a dose-dependent manner. WECG dose-dependently reduced histamine release from rat peritoneal mast cells and human mast cells. The inhibitory effect of WECG on histamine release was mediated by the modulation of intracellular calcium. In addition, WECG attenuated the phorbol 12-myristate 13-acetate and calcium ionophore A23187-stimulated gene expression and secretion of proinflammatory cytokines such as tumor necrosis factor- α and interleukin-6 in human mast cells. The inhibitory effect of WECG on these proinflammatory cytokines was nuclear factor- κB (NF- κB) dependent. Our findings provide evidence that WECG inhibits mast cell-derived allergic inflammation and involvement of calcium and NF- κB in these effects.

Publisher

SAGE Publications

Subject

General Biochemistry, Genetics and Molecular Biology

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