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Title 

2-Hydroxy-3-methoxybenzoic acid attenuates mast cell-mediated allergic reaction in mice via modulation of the FcεRI signaling pathway

Authors 

Y Y KimI G JeM J KimB C KangY A ChoiM C BaekB LeeJ K ChoiH R ParkT Y ShinSoyoung LeeSeung-Bin YoonSang-Rae LeeD KhangS H Kim

Publisher 

Nature Publishing Group

Issue Date 

2017

Citation 

Acta Pharmacologica Sinica

Keywords 

allergic inflammationhigh affinity IgE receptorhistamineo-vanillic acidpro-inflammatory cytokinerat peritoneal mast cellsRBL-2H3 cellstype I hypersensitivity

Abstract 

Mast cells are important effector cells in immunoglobulin (Ig) E-mediated allergic reactions such as asthma, atopic dermatitis and rhinitis. Vanillic acid, a natural product, has shown anti-oxidant and anti-inflammatory activities. In the present study, we investigated the anti-allergic inflammatory effects of ortho-vanillic acid (2-hydroxy-3-methoxybenzoic acid, o-VA) that was a derivative of vanillic acid isolated from Amomum xanthioides. In mouse anaphylaxis models, oral administration of o-VA (2, 10, 50 mg/kg) dose-dependently attenuated ovalbumin-induced active systemic anaphylaxis and IgE-mediated cutaneous allergic reactions such as hypothermia, histamine release, IgE production and vasodilation; administration of o-VA also suppressed the mast cell degranulator compound 48/80-induced anaphylaxis. In cultured mast cell line RBL-2H3 and isolated rat peritoneal mast cells in vitro, pretreatment with o-VA (1-100 μmol/L) dose-dependently inhibited DNP-HSA-induced degranulation of mast cells by decreasing the intracellular free calcium level, and suppressed the expression of pro-inflammatory cytokines TNF-α and IL-4. Pretreatment of RBL-2H3 cells with o-VA suppressed DNP-HSA-induced phosphorylation of Lyn, Syk, Akt, and the nuclear translocation of nuclear factor-κB. In conclusion, o-VA suppresses the mast cell-mediated allergic inflammatory response by blocking the signaling pathways downstream of high affinity IgE receptor (Fc?RI) on the surface of mast cells.

ISSN 

1671-4083

Link 

http://dx.doi.org/10.1038/aps.2016.112

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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