• IMMUNE NETWORK
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• v.4 no.3
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• pp.176-183
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• 2004

Background: Human seminal plasma (HSP)-induced hypersensitivity is one of the serious complications with sexual intercourse. The clinical manifestations of HSP-induced hypersensitivity may be related to the release of vasoactive mediators from mast cell induced by HSP. It has recently been reported that HSP modulates immune systems and induces mast cell degranulation and histamine release from rat peritoneal mast cells (RPMC). Ketotifen and disodium cromoglycate (DSCG), anti-asthmatic and anti-allergic drugs, have a role of mast cell stabilization and inhibit mast cell-induced leukocyte rolling and adhesion. But the inhibitory agents of HSP-induced mast cell activation are unknown. This study was performed to investigate the effects of DSCG and ketotifen on the HSP-induced mast cell activation. Methods: For this, influences of DSCG and ketotifen on the human seminal plasma-induced degranulation, histamine release and morphological changes of RPMC were observed. Results: The mast cell degranulation and histamine release of RPMC by HSP were induced in a dose-dependent fashion. The HSP-induced cytomorphological changes such as swelling, intracellular vacoules, and interrupted cell boundary were significantly inhibited by pretreatment with DSCG or ketotifen. DSCG and Ketotifen inhibited the HSP-induced degranulation and histamine release from RPMC. Conclusion: From the above results, it is suggested that DSCG and ketotifen have a inhibitory effect of the HSP-induced mast cell activation. DSCG and ketotifen may be used for treatment of HSP-induced hypersensitivity.

• Natural Product Sciences
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• v.17 no.3
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• pp.239-244
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• 2011

Immediate-type hypersensitivity is involved in many allergic diseases such as asthma, allergic rhinitis and anaphylaxis. The discovery of drugs for the treatment of allergic disease is an important subject in human health. Stimulation of mast cells releases inflammatory mediators, such as histamine and pro-inflammatory cytokines with immune regulatory properties. We investigated the effect of the aqueous extract of Schizonepeta tenuifolia (AEST) (Labiatae) on the immediate-type allergic reaction. AEST inhibited compound 48/80-induced systemic allergic reaction. AEST attenuated immunoglobulin E (IgE)-mediated skin allergic reaction and histamine release from human mast cell line (HMC-1) cells. In addition, AEST decreased the gene expression and secretion of pro-inflammatory cytokines in phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore A23187 (A23187)-stimulated HMC-1 cells. Our results indicate that AEST inhibits the mast cell-derived allergic reactions and involvement of histamine and pro-inflammatory cytokines in these effects.

• Journal of Microbiology and Biotechnology
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• v.12 no.3
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• pp.483-489
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• 2002

The role of $G{\alpha}12\;and\;G{\alpha}13$ in modulating the IgE receptor-mediated histamine secretion in the streptolysin-o-permeabilized human cultured mast cell was investigated. The expression of $G{\alpha}12\;and\;G{\alpha}13$ proteins were regulated during human cultured mast cell differentiation, and a significant correlation was observed between the levels of expression of $G{\alpha}12\;and\;G{\alpha}13$ proteins and IgE receptor-mediated histamine secretion capability in human cultured mast cells. Antibodies against $G{\alpha}12\;and\;G{\alpha}13$ effectively inhibited the IgE receptor-induced histamine release, and the concentration of anti-$G{\alpha}12$ antibody used to inhibit histamine secretion was shown to also inhibit the IgE receptor-mediated elevation of intracellular $Ca^2+$. Therefore, the results suggest that $G{\alpha}12\;and\;G{\alpha}13$ play roles in modulating IgE receptor-activated $Ca^2+$ influx, thereby regulating histamine release in cultured human mast cells. This is the first report to show that $G{\alpha}12\;and\;G{\alpha}13$ are involved in the regulation of $Ca^2+$ mediated exocytosis in human cultured mast cells.

• 대한약리학회:학술대회논문집
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• 2006.11a
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• pp.68.1-68.1
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• 2006

• The Korea Journal of Herbology
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• v.25 no.3
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• pp.35-41
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• 2010

Objectives : Allergy is an immune dysfunction caused by degranulation from mast cells in the early phase of allergic disease including allergic rhinitis (AR). The purpose of this study was to investigate the effects of Osterici Radix, roots of Ostericum koreanum Maximowicz in human mast cells and experimental allergic animal models. Methods : The anti-allergic effect of Osterici Radix water extract (NK-W) was investigated in human mast cell line, HMC-1 cells, and compound 48/80-induced systemic anaphylactic response in rats and ovalbumin (OVA)-induced AR in mice. Animals were orally administrated with NK-W (10 and 50 mg/kg) or anti-histamine drug, dosodium cromoglycate (50 mg/kg), and then intraperitoneally injected with compound 48/80 (8 mg/kg) or sensitized with 0.1% OVA into nasal. Animals were observed plasma histamine and histological changes of nasal mucosa. Also, mast cell degranulation and histamine production were determined in compound 48/80-stimulated HMC-1 cells. Results : NK-W inhibited compound 48/80-induced degranulation of mast cells and histamine releasing in HMC-1 cells. NK-W decreased mortality and serum histamine releasing in compound 48/80-induced anaphylatic rats in a dose-dependently manner. NK-W also inhibited serum histamine levels in OVA-induced AR mice and improved abnormal histological changes such as expansion of grandular cells and hypertrophy of epithelium in the nasal mucosa. These results indicate that Osterici Radix water extract suppress allergic response through downregulation of mast cell activation. Conclusions : This study suggests that a therapeutic potential of Osterici Radix as a source of anti-allergic agents for use in a number of allergic diseases.

• Biomedical Science Letters
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• v.13 no.2
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• pp.149-152
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• 2007

Mast cells play important roles in immune-related diseases, in particular, allergic diseases. Although 9-cis retinoic acid (9CRA) has been known as an immune regulator, its function in mast cells is not characterized well. In a previous paper, we demonstrated that 9CRA differentially decreases both CCR2 expression and the MCP-1-induced chemotactic activity of the human mast cell line, HMC-1 cells. In the present study, we examined the effects of 9CRA on the migration and expressions of inflammatory cytokines in HMC-1 cells. It was found that 9CRA significantly inhibited the migration of HMC-1 cells in response to stem cell factor (P<0.01), and it had no effect on the mRNA and protein expression of c-kit, a receptor binding to SCF. We further investigated the alternation of inflammatory cytokine expression and identified that 9CRA blocked the mRNA and protein expressions of Th2 cytokines such as interleukin (IL)-4 and IL-5. Taken together, our results demonstrate that 9CRA blocks SCF-induced cell movement and the protein secretion of IL-4 and IL-5, and this indicates that 9CRA may have anti-inflammatory effects on mast cells.

• Korean Journal of Clinical Laboratory Science
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• v.37 no.1
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• pp.41-46
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• 2005

It is known that mast cells (MCs) are increased in H. pylori-infected gastritis and its increase is mediated by stem cell factor (c-kit ligand). To determine the mechanism of mast cell recruitment and activation by stem cell factor, weinvestigated the expression of stem cell factor receptor (c-kit) in H. pylori-positive and -negative gastric mucosa. Biopsy specimens from 16 H. pylori-negative and 20 positive subjects were examined. H. pylori infection in gastric mucosa was examined by the Warthin-Starry method. MC and c-kit were identified by immunohistochemisty, using a monoclonal antihuman MC tryptase antibody and a polyclonal anti-human c-kit antibody. Densities of MC and c-kit positive cell were measured by a computerized image analysis system. MCs were detected in the lamina propria of both H. pylori-positive and -negative gastric mucosa. Densities of MC and c-kit positive cell were significantly greater in H. pylori-positive than -negative subjects. c-kit was located on the surface of MCs. These results indicate that stem cell factors may be one of the factors involved in mast cell increase and that they activate mast cells by binding with c-kit.

• YAKHAK HOEJI
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• v.49 no.5
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• pp.386-391
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• 2005

The discovery of drugs for the treatment of mast cell-mediated allergic disease is a very important subject in human health. The Amomum xanthiodes (Zingiberaceae) has been used for centuries as a traditional medicine in Korea and is known to have an anti-inflammatory effect. However, its specific mechanism of action is still unknown. In this report, we investigated the effect of hot water extract from Amomum xanthiodes (EAX) on the mast cell-mediated allergic reaction and studied its possible mechanisms of action. EAX inhibited compound 48/80-induced systemic anaphylaxis and serum his­tamine release in mice. EAX decreased the passive cutaneous anaphylaxis reaction activated by anti-dinitrophenyl (DNP) IgE antibody. EAX dose-dependently reduced histamine release from rat peritoneal mast cells activated by compound 48/80 or anti-DNP IgE. EAX increased cAMP and decreased compound 48/80-induced intracellular $Ca^{2+}$ levels. Our findings provide evidence that EAX inhibits mast cell-derived allergic reactions, and also demonstrate the involvement of cAMP and intracellular $Ca^{2+}$ in these effects.

• Journal of Evidence-Based Herbal Medicine
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• v.1 no.1
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• pp.13-18
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• 2008

Polygoni cuspidati Rhizoma (PCRH) has been used in treatment of menoxenia, skin burn, gallstone, hepatitis, hyperlipidaemia, favus athlete's foot, supperative dermatitis and inflammation. However, its effect in experimental models remains unknown. In this present study, the effect of PCRH for stability on mast cell was analyzed. Two g/kg PCRH inhibited the compound 48/80-induced anaphylaxis by 75%. In addition, PCRH inhibited the tumor necrosis factor-$\alpha$ and interleukin-8 secretion as compared with the phorbol 12-myristate 13-acetate plus calcium ionophore A23187 stimulated human mast cell line, HMC-1 cells. These results suggested PCRH may inhibit mast cell-mediated anaphylactic reaction.

• Natural Product Sciences
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• v.23 no.1
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• pp.1-4
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• 2017

Sinensetin, a pentamethoxyflavone, is known to exert various pharmacological activities including anti-angiogenesis, anti-diabetic and anti-inflammatory activities. However, its effects on the human mast cell - 1 (HMC-1) mediated inflammatory mechanism remain unknown. To explore the mediator and cellular inflammatory response of sinensetin, we examined its influence on phorbol 12-myristate 13-acetate (PMA) plus A23187 induced inflammatory mediator production in a human mast cell line. In this study, interleukin (IL)-6 production was measured using the enzyme-linked immunosorbent assay and reverse transcription polymerase chain reaction. Sinensetin inhibited PMA plus A23187 induced IL-6 production in a dose-dependent manner as well as IL-4, IL-5 and IL-8 mRNA expression. Furthermore, sinensetin inhibited signal transducer and activator of transcription 3 (STAT3) phosphorylation, suggesting that sinensetin inhibits the production of inflammatory mediators by blocking STAT3 phosphorylation. Moreover, sinensetin was found to inhibit nuclear factor kappa B activation. These findings suggest that sinensetin may be involved in the regulation of mast cell-mediated inflammatory responses.