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Sparassis crispa suppresses mast cell-mediated allergic inflammation: Role of calcium, mitogen-activated protein kinase and nuclear factor-κB
Author(s) -
Hui-Hun Kim,
Soyoung Lee,
Thoudam S.K. Singh,
Jin Kyeong Choi,
TaeYong Shin,
SangHyun Kim
Publication year - 2012
Publication title -
international journal of molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.048
H-Index - 90
eISSN - 1791-244X
pISSN - 1107-3756
DOI - 10.3892/ijmm.2012.1000
Subject(s) - histamine , mast cell , tumor necrosis factor alpha , protein kinase a , immunoglobulin e , immunology , allergic inflammation , proinflammatory cytokine , inflammation , p38 mitogen activated protein kinases , chemistry , kinase , pharmacology , medicine , antibody , biochemistry
Allergic inflammatory disease such as food allergy, asthma and atopic dermatitisare increasing worldwide. In this study, we investigated the effect of water extractof Sparassis crispa (WESC) Fr. (Aphyllophoromycetideae) on mast cell-mediatedallergic inflammation and the possible mechanisms of action. WESC inhibited compound48/80-induced systemic anaphylaxis and serum histamine release in mice. WESC decreasedimmunoglobulin E (IgE)-mediated passive cutaneous anaphylaxis. Additionally, WESCreduced histamine release and intracellular calcium in human mast cells activatedby phorbol 12-myristate 13-acetate (PMA) and calcium ionophore A23187. WESC decreasedPMA and A23187-stimulated expression of pro-inflammatory cytokines, such as tumornecrosis factor (TNF)-α, inlerleukin (IL)-6 and IL-1β. The inhibitory effect ofWESC on pro-inflammatory cytokines was nuclear factor-κB, extracellular signal-regulatedkinase and p38 mitogen-activated protein kinase-dependent. Our results suggestpotential therapeutic application of WESC in allergic inflammatory diseases.

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