Vigna angularis inhibits mast cell-mediated allergic inflammation

Kim,Hui-Hun; Kim,Sung-Wan; Kim,Duk-Sil; Oh,Hyun-Mee; Rho,Mun-Chual; Kim,Sang-Hyun

doi:10.3892/ijmm.2013.1430

Vigna angularis inhibits mast cell-mediated allergic inflammation

Authors:
- Hui-Hun Kim
- Sung-Wan Kim
- Duk-Sil Kim
- Hyun-Mee Oh
- Mun-Chual Rho
- Sang-Hyun Kim
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Affiliations: Korean Traditional Medicine Agency, Korea Promotion Institute for Traditional Medicine Industry, Gyeongsan 712‑210, Republic of Korea, Department of Thoracic and Cardiovascular Surgery, CHA Gumi Medical Center, CHA University, Gumi 730-040, Republic of Korea, Bioindustrial Process Research Center, Bio-Materials Research Institute, Korea Research Institute of Bioscience and Biotechnology, Jeongeup 580-185, Republic of Korea, Cell and Matrix Research Institute (CMRI), Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 700-422, Republic of Korea
Published online on: July 4, 2013 https://doi.org/10.3892/ijmm.2013.1430
Pages: 736-742

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Abstract

The aim of the present study was to elucidate whether extracts of Vigna angularis (EVA) inhibit allergic inflammatory reactions and to elucidate the possible mechanisms of action. For the assessment of allergic inflammatory response, histamine release and the expression of pro-inflammatory cytokines from human mast cells (HMC-1) were examined. To identify the underlying mechanisms of action, intracellular calcium and the activation of nuclear factor (NF)-κB and mitogen-activated protein kinases (MAPKs) were assayed. To confirm the effects of EVA in vivo, systemic and local allergic reaction mouse models were employed. EVA dose-dependently reduced phorbol 12-myristate 13-acetate and calcium ionophore A23187 (PMACI)-induced histamine release from mast cells. The inhibitory effects of EVA on the release of histamine from mast cells were mediated by the reduction of intracellular calcium levels. EVA decreased the PMACI-stimulated gene expression and secretion of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6. The inhibitory effects of EVA on pro-inflammatory cytokines were NF-κB- and MAPK-dependent. In addition, EVA inhibited compound 48/80-induced systemic anaphylaxis and immunoglobulin E (IgE)-mediated cutaneous anaphylaxis. Our findings provide evidence that EVA inhibits mast cell-derived allergic inflammation, and suggest the possible therapeutic application of EVA in allergic inflammatory disorders.

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