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Diospyros kaki (D. kaki) has been cultivated throughout Eastern Asia for hundreds of years. D. kaki contains various biological active compounds, such as amino acids, carotenoids, flavonoids, tannins, catechins and vitamin A. Previous studies have shown that D. kaki has beneficial effects on homeostasis, constipation, hypertension, atherosclerosis and allergic dermatitis and is a good source of antioxidants, polyphenols and dietary fiber. However, the anti-allergic and anti-inflammatory effects of D. kaki have not yet been elucidated. This study aimed to investigate the protective effects of the aqueous extract of Diospyros kaki (AEDK) on mast cell-mediated allergic inflammation and to determine its possible mechanisms of action by using in vitro and in vivo mast cell-based models. The cAMP and intracellular calcium levels were measured to clarify the mechanisms by which AEDK inhibits the release of histamine from mast cells. AEDK inhibited the release of histamine and β-hexosaminidase from mast cells by modulating cAMP and intracellular calcium levels. We also measured the expression of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β. AEDK decreased gene expression and the secretion of the pro-inflammatory cytokines, TNF-α and IL-1β by inhibiting nuclear factor-κB. In addition, AEDK inhibited systemic and cutaneous allergic reaction. The inhibitory effects of AEDK on allergic reaction and the release of histamine were found to be similar to those of disodium cromoglycate, a known anti-allergic drug. To isolate the active component of AEDK, activity-guided fractionation was performed, based on the inhibitory effects on systemic anaphylaxis. Catechin was identified as an active compound. The present findings provide evidence that AEDK inhibits allergic inflammation and suggest the therapeutic application of AEDK in allergic inflammatory disorders.

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.

Piceatannol is a phenolic stilbenoid and a metabolite of resveratrol which is found in red wine. Piceatannol (PIC) commonly exhibits anti-inflammatory, antiplatelet and antiproliferative activity. In the present study, the anti-allergic and anti-inflammatory mechanisms of PIC were investigated by examining the effects of PIC on pro‑inflammatory cytokine release and phosphorylation of mitogen-activated protein (MAP) kinases (ERK, JNK and p38) in a human mast cell line. PIC dose-dependently inhibited compound 48/80-induced systemic anaphylaxis and immunoglobulin E-mediated local allergic reactions. PIC reduced the immunoglobulin E (IgE)-mediated local allergic reaction and attenuated histamine release from rat peritoneal mast cells. Histamine and β-hexosaminidase release was markedly decreased dose-dependently by PIC treatment in RBL-2H3 cells. PIC treatments of HMC-1 cells definitely reduced mRNA expression and the release of the pro‑inflammatory cytokines, tumor necrosis factor-α and interleukin-8. MAP kinase phosphorylation was also strongly decreased dose-dependently following PIC treatment. PIC regulated the production of cytokines and histamine in phorbol 12-myristate 13-acetate plus A23187-stimulated mast cells. Thus, PIC may alleviate allergic inflammation and may be a useful therapeutic agent for allergic diseases.

Allergic inflammatory disease such as food allergy, asthma and atopic dermatitis are increasing worldwide. In this study, we investigated the effect of water extract of Sparassis crispa (WESC) Fr. (Aphyllophoromycetideae) on mast cell-mediated allergic inflammation and the possible mechanisms of action. WESC inhibited compound 48/80-induced systemic anaphylaxis and serum histamine release in mice. WESC decreased immunoglobulin E (IgE)-mediated passive cutaneous anaphylaxis. Additionally, WESC reduced histamine release and intracellular calcium in human mast cells activated by phorbol 12-myristate 13-acetate (PMA) and calcium ionophore A23187. WESC decreased PMA and A23187-stimulated expression of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, inlerleukin (IL)-6 and IL-1β. The inhibitory effect of WESC on pro-inflammatory cytokines was nuclear factor-κB, extracellular signal-regulated kinase and p38 mitogen-activated protein kinase-dependent. Our results suggest potential therapeutic application of WESC in allergic inflammatory diseases.

In this study, we investigated the effect of a water extract of the ripe fruits of Rubus coreanus Miq. (Rosaceae) (RFRC) on mast cell-mediated allergic inflammation and studied the possible mechanism of action. Mast cell-mediated allergic disease is involved in many diseases such as anaphylaxis, rhinitis, asthma and atopic dermatitis. RFRC dose-dependently inhibited compound 48/80-induced systemic anaphylaxis and serum histamine release in mice. RFRC reduced the immunoglobulin E (IgE)-mediated local allergic reaction, passive cutaneous anaphylaxis. RFRC attenuated histamine release from rat peritoneal mast cells and human mast cells by the reduction of intracellular calcium. RFRC decreased the phorbol 12-myristate 13-acetate (PMA) and the calcium ionophore A23187 (PMACI)-stimulated expression and secretion of pro-inflammatory cytokines in human mast cells. The inhibitory effect of RFRC on cytokine production was nuclear factor (NF)-κB- and mitogen-activated protein kinase (MAPK)-dependent. In addition, RFRC suppressed the activation of caspase-1. Our findings provide evidence that RFRC inhibits mast cell-derived allergic inflammatory reactions, and for the involvement of calcium, NF-κB, MAPKs and caspase-1 in these effects. Furthermore, in vivo and in vitro anti-allergic inflammatory effects of RFRC provide affirmative proof of a possible therapeutic application of this agent in allergic inflammatory diseases.