• The Korean Journal of Physiology
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• v.22 no.2
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• pp.259-272
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• 1988

Type I allergic reaction and it's related clinical manifestations are known to occur by the effects of various chemical mediators. These chemical mediators are released from circulating basophils and tissue mast cells, which become 'sensitized' through the binding of antigens and antibodies of the IgE type to their cell surface receptors. Efforts to elucidate the mechanism of the release of these mediators, especially that of histamine, have been persued for years. The mechanism is not yet clarified at the present time. Recent reports of hyaluronidase, an enzyme known to be involved in the tissue inflammatory process, as possible participant in type I allergic reaction, initiated this study. Relationships between the hyaluronidase activity and histamine release from the sensitized rat peritoneal mast cells were investigated. Also anti-allergic agents, tranilast and disodium cromoglycate, along with known histamine releasers, morphine and compound 48/80, were used to observe the inhibitory and stimulatory effects of these substances on the hyaluronidase activity as well as histamine release from the rat mast cells. The results obtained are summarized as follows: 1) Hyaluronidase activity and histamine release from sensitiaed rat peritoneal mast cells started to increase on the 4th day of postsensitization. Hyaluronidase activity reached it's peak value on the 7th day of postsensitization and that of histamine release on the 14th day of postsensitization. 2) Hyaluronidase activity and histamine release from sensitized rat peritoneal mast cells, pre-treated with tranilast revealed significant decrease in comparison with those of non-treated cells. 3) Hyaluronidase activity and histamine release from sensitized rat peritoneal mast cells, pre-treated with tranilast, followed by morphine injection, revealed significant increase in comparison with those of tranilast treated cells. 4) In vitro study of hyaluronidase activity and histamine release from un-sensitized rat peritoneal mast cells, using morphine and compound 48/80 as activators, revealed significant increase compared to those of non-activator used cells. 5) In vitro study of hyaluronidase activity and histamine release from un-sensitized rat peritoneal mast cells, pre-treated with tranilast and disodium cromoglycate, using confound 48/80 and morphine as activators revealed significant decrease in comparison with those of tranilast and disodium cromoglycate treated cells. From above results, participation of enzyme hyaluronidase in the process of histamine release from sensitized rat pertioneal mast cells, could be suggested. It was also quite evident that the clinically used anti-allergic agents, tranilast and disodium cromoglycate, have significant inhibitory function on the hyaluronidase activity and histamine release from sensitized rat peritoneal mast cells, while morphine significantly increased the hyaluronidase activity and histamine release from sensitized rat peritoneal mast cells.

• YAKHAK HOEJI
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• v.39 no.6
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• pp.616-621
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• 1995

The effect of WK101 on compound 48/80-induced anaphylaxis was studied in rat. WK101 was found to exhibit a inhibitory activity on the compound 48/80-induced anaphylaxis. WK101 also inhibited the serum histamine release induced in anaphylaxis by compound 48/80. The effect of WK101 on the histamine release from rat peritoneal mast cells was studied. WK101 ($10^{3}-1mg/ml$) inhibited the histamine release induced by compound 48/80($5{\;}\mu\textrm{g}/ml$) in rat peritoneal mast cells. To clarify the mechanism of these inhibitons, we investigated the effects of WK101 on cAMP and intracellular calcium content of rat peritoneal mast cell. The content of cAMP in mast cells, when WK101 was added, was increased transiently, and was significantly increased more 53 fold at 10 sec than that of basal cells. Moreover, WK101 inhibited intracellular calcium release induced by compoound 48/80. This results suggest that WK101 may be useful for the prevention and treatment of allergy-related disease.

• YAKHAK HOEJI
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• v.41 no.5
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• pp.652-657
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• 1997

We studied the effects of sulfasalazine(SSZ) on anaphylaxis. SSZ was found to exhibit a inhibitory activity on the compound 48/80-induced anaphylaxis. SSZ also inhibited local a naphylaxis activated by anti-dinitrophenyl(DNP) IgE. Moreover, SSZ dose-dependently inhibited histamine ralease in rat peritoneal mast cells activated by compound 48/80 or anti DNP IgE. We investigated the effects of SSZ on cAMP of rat peritoneal mast cell. The level of cAMP in rat peritoneal mast cells, when SSZ was added, transiently and significantly increased approximately 16-fold compared with that of basal cells. These results suggest that the antianaphylactic action of SSZ may be associated with an increase in the intracellular cAMP content of the mast cells as the result of an inhibition of the cAMP phosphodiesterase.

• YAKHAK HOEJI
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• v.45 no.6
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• pp.677-682
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• 2001

investigate action of ethanol on histamine release from rat peritoneal mast cells, we compared the inhibitory effect of ethanol with those of calcium antagonists in mechanism of between ATP and compound 48/80-induced histamine release. Ethanol dose-dependently inhibited 100 ${\mu}{\textrm}{m}$ ATP-induced histamine release, whereas did not inhibit 1 $\mu\textrm{g}$/ml compound 48/80-induced histamine release. Verapamil, TMB-8 and EGTA dose-dependently inhibited ATP-induced histamine release, but did not inhibit compound 48/80-induced histamine release. Such an inhibitory effect of calcium antagonist was similar to that of ethanol. These results suggest that the inhibitory effect of ethanol on histamine release from rat peritoneal mast cells is mediated via disturbance of calcium mobilization..

• Korean Journal of Plant Resources
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• v.24 no.1
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• pp.98-104
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• 2011

We investigated inhibitory effects of ginseng extracts against compound 48/80-induced responses in rat peritoneal mast cells. Initially, we optimized extraction condition with various temperature and time for recovery of high saponin contents in extracts. Using a primary rat peritoneal mast cells, we examined whether ginseng extracts inhibit compound 48/80-induced histamine release form rat mast cells. High red ginseng-spercific saponin containing extracts were recovered at $85^{\circ}C$ for 48 hr, and had no cytotoxicity with relatively high dose of extracts on rat peritoneal mast cells(<0.5 mg/ml). For examine of ameliorate effects of mast cells responses by ginseng extract, we pre-treated the extracts or saline to mast cells and treated compound 48/80. In results, compound 48/80 treatment was increased histamine release (approximately 30%) from mast cells than normal group, whereas ginseng treatment was completely inhibited histamine release. These results suggested that ginseng extracts inhibits the compound 48/80-induced mast cell activation, and ginseng extracts is a candidate for effective therapeutic tools of allergic diseases.

• YAKHAK HOEJI
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• v.42 no.3
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• pp.319-323
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• 1998

Effects of the aqueous extract of Cryptotympana atrata Fabricius (CAF) on the allergic reactions were investigated. In the present study, we examined the effect of CAF on compound 48/80-induced anaphylaxis in vivo and histamine release from rat peritoneal mast cells in vitro. CAF dose-dependently inhibited systemic anaphylaxis induced by compound 48/80 in mice. CAF significantly inhibited serum histamine levels induced by compound 48/80. CAF also inhibited histamine release from the rat peritoneal mast cells activated by compound 48/80. These results suggest that CAF may be useful for the prevention and treatment of allergy related disease.

• Preventive Nutrition and Food Science
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• v.11 no.2
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• pp.89-93
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• 2006

Methanol extracts (80%, $10{\mu}g/mL$) of Actinidia chinensis (AC) and Zizyphus jujube(ZJ) inhibited histamine release from rat peritoneal mast cells (RPMCs) induced by compound 48/80. Evaluation of AC and ZJ solvent fractions (chloroform, ethylacetate, butanol and water) revealed that the butanol fraction of AC at $5{\mu}g/mL$ and water fraction of ZJ at $1{\mu}g/mL$ exhibited the highest anti-allergic effects. Combination of the butanol fraction of AC and water fraction of ZJ when combined showed higher inhibition of histamine release than either alone. The levels of cAMP in RPMCs treated with AC and ZJ were significantly increased compared to the compound 48/80 treated control. Our findings suggest that the extracts from AC and ZJ may alleviate immediate hypersensitivity reactions through the increase of cAMP in the mast cells.

• Archives of Pharmacal Research
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• v.22 no.2
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• pp.108-112
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• 1999

Recombinant murine stem cell factor (rmSCF) or recombinant murine nerve growth factor (rmNGF) induced the morphological change of large numbers of rat peritoneal mast cells (RPMC). We investigated the role of phosphatidylinositol $3^{l}-kinase$ (PI3-kinase) in receptors-mediated morphological change in RPMC. Exposure of RPMC to PI3-kinase inhibitor, wortmannin, before the addition of rmSCF and rmNGF antagonized those factors-induced morphological change. These results suggest that the PI3-kinase is involved in the signal transduction pathway responsible for morphological change following stimulation of rmSCF and rmNGF and that wortmannin blocks these responses.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.194.1-194.1
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• 2003

Phenylpropanoids originating from vegetable kingdom have some biological activity. In this experiments, effect of phenylpropanoids on the histamine release from mast cells were studied in vitro. Rat peritoneal mast cells were isolated by the discontineous gradients of Percoll and their histamine release by stimulation of compound 48/80 and A23187 at a concentration of 6.0 $\mu\textrm{g}$/$m\ell$ were determined. (omitted)

• Advances in Traditional Medicine
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• v.1 no.1
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• pp.82-88
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• 2000

We investigated the effect of aqueous extract of Cichorium intybus (CIAE) on mast cell-mediated immediate type allergic reactions. CIAE dose-dependently inhibited systemic anaphylactic reaction induced by compound 48/80 in mice. Especially, CIAE inhibited compound 48/80-induced anaphylactic reaction 100% with the dose of 1000 mg/kg. CIAE 1000 mg/kg also significantly inhibited local anaphylactic reaction activated by anti-dinitrophenyl (DNP) IgE. When mice were pretreated with CIAE at a concentration ranging from 0.1 to 1000 mg/kg, the plasma histamine levels were reduced in a dose-dependent manner. CIAE (1 to 1000 g/ml) dose-dependently inhibited histamine release from the rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. These results indicate that CIAE inhibits mast cell-mediated immediate-type allergic reactions.