• Proceedings of the PSK Conference
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• 2000.04a
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• pp.138-138
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• 2000

• Journal of the korean academy of Pediatric Dentistry
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• v.28 no.1
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• pp.72-81
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• 2001

Dendroaspis natriuretic peptide (DNP), recently isolated from the venom of the green Mamba snake Dendroaspis angusticeps, is a 38-amino acid peptide containing a 17-amino acid disulfide ring structure similar to that of the natriuretic peptide family. The natriuretic peptide family was known to induce histamine release from human and rat mast cells, but there are no published data concerning the effects of DNP on histamine release from mast cells. The purpose of this study is to investigate whether DNP induces the histamine release from rat peritoneal mast cells (RMPCs) and to determine the mechanism of DNP-induced histamine release from RPMCs. After treatment of the various doses of DNP in RPMCs, the mast cell degranulation was observed with inverted microscopy and the histamine release was measured by radio-enzymatic assay. Calcium uptake and intracellular cyclic GMP level were measured by radioimmunoassays. DNP induced the mast cell degranulation. DNP released the histamine and increased the calcium uptake and the level of intracellular cyclic GMP of RPMCs, in a dose-dependent manner. The results indicate that DNP is capable of inducing histamine release from RPMCs by increasing of calcium uptake and intracellular cyclic GMP level.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2003.11a
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• pp.76-76
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• 2003

Mast cells accumulation can be causally related with several allergic inflammations. Previous work has demonstrated that glucocorticoids decreased tissue mast cell number and stem cell factor (SCF)-induced migration of mast cells required p38 mitogen-activated protein kinase (MAPK) activation. In the present study, we investigated the effects of dexamethasone on SCF-induced migration of rat peritoneal mast cells (RPMCs). SCF significantly induced migration of RPMCs at 4 h. Dexamethasone dose-dependently inhibited SCF-induced migration of RPMCs (about 90.1% at 100 nM, P<0.05). MAPK p38 inhibitor, SB203580 (20 ${\mu}$M) also inhibited the SCF-induced migration. The ability of SCF to enhance morphological alteration and F -actin formation was also abolished by treatment of dexamethasone. Dexamethasone inhibited SCF-induced p38 MAPK activation to near basal level and induced the MKP-1 expression. In addition, SCF-induced inflammatory cytokine production was significantly inhibited by treatment of dexamethasone or SB203580 (p<0.01). Our results show that dexamethasone potently regulates SCF -induced migration, p38 MAPK activation and inflammatory cytokine production through expression of MKP-l protein in RPMCs. Such modulation may have functional consequences during dexamethasone treatment, especially mast cell-mediated allergic inflammation disorders.

• YAKHAK HOEJI
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• v.41 no.2
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• pp.255-259
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• 1997

Effects of the aqueous extract of Aquilariae Lignum (Thymelaeaceae) on the allergic reactions were investigated. Oral administration of this extract (50, 250, and 500mg/kg) exhi bited a dose-dependent inhibition on passive cutaneous anaphylactic reactions in rats. Administrations of this extract (500mg/kg, i.p.) at 60 min before and 5, 10 min after the compound 48/80 treatment (8mg/kg, i.p.) decreased the mortality rates to 0, 0, and 14.2%, respectively. The aqueous extract of Aquilariae Lignum (0.05 ~ 1.6mg/ml) showed a dose-related inhibition on histamine release from rat peritoneal mast cells. The morphological examination also clearly showed that the aqueous extract of Aquilariae Lignum prevented the degranulation of mast cells in rats.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.14 no.2
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• pp.231-241
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• 2001

Mahwang-Shin-Gung-San has been found inhibiting the mast cell-mediated anaphylactic reaction. This report describes an inhibitory effect of Mahwang-Shin-Gung-San (MSGS) on the immediate-type cutaneous allergic reactions. MSGS has concentration -dependently inhibited the ear swelling response induced by compound 48/80 in mouse by intradermal injection. The mast cells in mouse ear tissue undergone ear-swelling response by compound 48/80 were stained by alcian blue/nuclear fast red. MSGS significantly inhibited the compound 48/80-induced degranulation from mast cells in ear tissue. MSGS concentration-dependently inhibited the histamine release from the rat peritoneal mast cells (RPMC) by compound 48/80. We also studied the effect of MSGS on mast cell-dependent passive cutaneous anaphylaxis (PCA) activated by dinitrophenyl IgE antibody. MSGS showed potent inhibition of PCA by oral administration. These results indicate that MSGS inhibits immediate-type allergic reactions by inhibition of mast cell degranulation in vivo and in vitro.

• Archives of Pharmacal Research
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• v.24 no.6
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• pp.552-556
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• 2001

Histamine and arachidonic acid (AA) release was measured using the P2-purinoceptor antaongists, phospholipase $A_2{\;}(PLA_2)$ and cyclooxygenase (COX)/lipoxygenase (LOX) inhibitors to determine whether or not ATP-induced histamine release is associated with arachidonic acid (AA) release in rat peritoneal mast cells. ATP increased histamine release in a dose dependent manner, whereas adenosine did not. PPADS (a selective P2X-purinoceptor antagonist) and suramin (a nonselective P2X,2Y-purinoceptor antagonist) inhibited ATP-induced histamine release in a dose dependent manner. However, RB-2 (a P2Y-purinoceptor antagonist) did not block ATP-induced histamine release. Manoalide and oleyloxyethyl phosphorylcholine (OPC), secretory PLA$_2$ inhibitors, also inhibited ATP-induced histamine release dose-dependently. Both COX inhibitors (ibuprofen and indomethacin) and LOX inhibitors (baicalein and caffeic acid) inhibited ATP-induced histamine in a dose dependent manner. ATP significantly increased [$^3H$]AA release by 54%. PPADS and suramin significantly inhibited ATP-induced [3H]Ph release by 81% and 39%, respectively. ATP-induced histamine release was significantly inhibited by a variety of protein kinase inhibitors, such as bisindolmaleimide, genistein, methyl 2,5-dihydroxycinnamate, W-7 and trifluoperazine. Overall, the results suggest that ATP-induced histamine release is in part related to the PLA2-mediated AA metabolism and P2X-purinoceptors.

• Natural Product Sciences
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• v.10 no.1
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• pp.24-28
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• 2004

The effects of aqueous extract of Artemisia iwayomogi (Compositae) (AIAE) on the mast cell-dependent allergic and inflammatory reactions were investigated. AIAE (0.05 to 1 g/kg) dose-dependently inhibited systemic allergic reaction induced by compound 48/80 in mice. AIAE (0.1 and 1 g/kg) also significantly inhibited local allergic reaction activated by anti-DNP IgE. AIAE (0.001 to 1 mg/ml) dose-dependently inhibited the histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80. Moreover, AIAE inhibited the secretion of interleukin (IL)-6 in phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore A23187-stimulated human mast cell line (HMC-1) cells. These results provide evidence that AIAE may be beneficial in the treatment of allergic diseases.

• The Journal of Internal Korean Medicine
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• v.25 no.2
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• pp.159-166
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• 2004

Objective : Mast cells are a potent source of mediators that regulate inflammatory response in allergies and asthma. The author studied the effect of Bojungikgitanggamibang(BITB) on mast cell-mediated anaphylactic reaction. Method : When BITB was given as pre-treatment at concentrations ranging from 0.01 to 1 mg/ml, the histamine release from rat peritoneal mast cells induced by compound 48/80 was reduced in a dose-dependent manner. Result : BITB dose-dependently inhibited compound 48/80-induced systemic anaphylactic shock. BITB also inhibited passive cutaneous anaphylaxis activated by anti-dinitrophenyl IgE. In addition, BITB inhibited phorbol 12-myristate 13-acetate and A23187-induced interleukin-6 secretion from human mast cell line HMC-1 cells. Conclusion : These results indicate that BITB may be actively anti-allergic.

• Journal of Sasang Constitutional Medicine
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• v.10 no.2
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• pp.589-613
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• 1998

The purpose of this research was to investigate effects of Bangpoongtongsungsan water extract(BTSE) on the immune reaction, anti-allergy action and anti-inflammatory action in BALB/c mice. The administration of BTSE (500mg/kg) enhanced the cell viability of thymocytes and the population of helper T cells in splenic T-lymphocytes. BTSE suppressed the production of nitric oxide, but enhanced the phagocytic activity in peritoneal macrophages. BTSE enhanced hemagglutination titer in mice. BTSE inhibited passive cutaneous anaphylaxis induced by egg albumin in rat, the lethal anaphylaxis induced by platelet activating factor and compound 48/80 in mice, and then inhibited the degranulation of peritoneal mast cells induced by compound 48/80. BTSE did not inhibit Arthus reaction, but inhibited the delayed type hypersensitivity induced by SRBC and contact dermatitis induced by DNFB. BTSE inhibited the acute hind paw edema induced by histamine after 30 minutes, the permeability of evans blue into peritoneal cavity induced by acetic acid and the writhing syndrome induced by acetic acid. These results suggest that BTSE has an immunopotentiative action, anti-allergy action and anti-inflammatory action via the inhibition of histamine release.

• 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.