• 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.

• IMMUNE NETWORK
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• v.10 no.1
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• pp.15-25
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• 2010

Background: Rat mast cells were regarded as a good model for mast cell function in immune response. Methods: Rat bone marrow mast cells (BMMC) were prepared both by recombinant rat IL-3 (rrIL-3) and by recombinant mouse stem cell factor (rmSCF), and investigated for both proliferation and differentiation in time course. Rat BMMC was induced by culture of rat bone marrow cells (BMCs) in the presence of both rrIL-3 (5 ng/ml) and rmSCF (5 ng/ml). Culture media were changed 2 times per week with the cell number condition of $5{\times}10^4/ml$ in 6 well plate. Proliferation was analyzed by cell number and cell counting kit-8 (CCK-8) and differentiation was by rat mast cell protease (RMCP) II and histamine. Results: Cell proliferation rates reached a maximum at 8 or 11 days of culture and decreased thereafter. However, both RMCP II production and histamine synthesis peaked after 11 days of culture. By real time RT-PCR, the level of histidine decarboxylase mRNA was more than 500 times higher on culture day 11 than on culture day 5. By transmission electron microscopy, the cells were heterogeneous in size and contained cytoplasmic granules. Using gated flow cytometry, we showed that cultured BMCs expressed high levels of $Fc{\varepsilon}RI$ and the mast cell antigen, ganglioside, on culture day 11. Conclusion: These results indicate that rat BMMCs were generated by culturing BMCs in the presence of rrII-3 and rmSCF and that the BMMCs have the characteristics of mucosal 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.

• Korean Journal of Veterinary Research
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• v.31 no.1
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• pp.77-87
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• 1991

In order to know the influence of mast cells on the mammary tumor development, the growth of the mammary carcinoma, the numerical changes and the morphological findings of mast cells appeared in the tumor were microscopically observed in the rat treated with DMBA and each chemical of histamine, heparin, pyrilamine or cimetidine. The results observed were summarized as follows: The tumor induction time that represented the number of days elapsing between the 3rd DMBA administration until a first tumor became $10{\times}10mm$ in diameter was $42.5{\pm}4.7$ days, and the mean number of tumor mass per rat was $3.4{\pm}1.2$ in the DMBA-treated group. No significant difference was apparent in the tumor induction time of the histamine-treated group, heparin-treated group or pyrilamine-treated group compared with the control group, but in the cimetidine-treated group the tumor induction time was $61.8{\pm}10.6$ days (p<0.005). The mean number of tumors per rat was $2.1{\pm}0.9$ in the cimetidine-treated group in contrast to $3.4{\pm}1.3$ in the control group (p<0.005). Numerical changes of mast cells were observed according to the development of DMBA induced mammary tumors that were separated into three major classes of tumors. The numbers of mast cells in all the experimental group were inclined to increase significantly according to the mammary tumor development (p<0.005), and the histamine-treated group, heparin-treated group, or pyrilamine-treated group were nearly similar to the control group. But the mast cells in the each stage of tumor development were more numerous in the cimetidine-treated group than in the control group (p<0.005). There were not significant in the numerical changes of mast cells among the experimental groups on each stage of carcinomas separated by early stage, middle stage and late stage. In the morphological characteristics of mast cells, the degranulation was not detectable from the hyperplasia stages to the early stage of carcinoma, but its degranulation was observed at the middle stage of carcinoma. Most mast cells were nearly degranulated at the late stage of carcinoma. The histamine treated group, pyrilamine-treated group and cimetidine treated group did not differ from the control group in morphological changes of mast cells, but the degranulation was shown mild in the heparin-treated group. And the degranulation gave rise to the depletion of intercellular matrix via exocytosis all the experimental group. From above results, it is supposed that mast cells inhibit the tumor development and that the inhibition is not caused by a single-factor, but by a complex activities of mast cell mediators.

• 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.

• The Korean Journal of Zoology
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• v.16 no.1
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• pp.13-23
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• 1973

The changes in the quantitative distribution and in cytoplasmic granules of tongue mast cells and duodenal enterochromaffin cells in male albino rats were observed following oral administration of 40mg/kg body wt. isonicotinic acid hydraside (INH) and 20mg/kg body wt. pyridoxine. The results obtained are summarized as follows: 1. INH administered-rat showed a marked decrease in the number of mast cells, caused by leakage of cytoplasmic granules, while pyridoxine-rat showed increased the number of mast cells. 2. Similarly, INH-rat showed a marked decrease in the number of enterochromaffin cells. In the case of pyridoxine-rat, however, the number of enterochromaffin cells increased compared with that of the controls. 3. In view of the fact that a large dose of INH was harmful to the formation of mast cells and enterochromaffin cells. And considering that a moderate dose of pyridoxine stimulated the formation of the two kinds of cells and the amounts of cytoplasmic granules, it was concluded that pyridoxine might be concerned with the metabolism of secretory products, 5-Hydroxytryptamine.

• Korean Journal of Veterinary Research
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• v.31 no.3
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• pp.343-353
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• 1991

In order to investigate the histopathological, mechanism of Rompun-induced shock, the development of mammary carcinoma, the numerical changes and the morphological findings of the mast cells appeared in the carcinoma were microscopically observed in the rat treated with DMBA and each chemical of compound 48/80 and Rompun. Also mast cell degranulation induced by Rompun was observed with electron microscope. The results observed were summarized as follows: Tumor appeared in 100% of the animals. Tumors grew more rapidly to $10{\times}10mm$ in rats depleted of mast cells ($37.7{\pm}4.2$ days) than was observed in the control group ($42.5{\pm}4.7$ days) (p<0.005). The mean number of tumors per rat was $2.8{\pm}1.3$ in the compound 48/80- treated group in contrast to $3.4{\pm}1.3$ in the control group. No significant difference was apparent in the tumor induction time of Rompun treated group compared with the compound 48/80-treated group, but the tumor measuring at least $10{\times}10mm$ appeared more quickly in the Rompun treated group than in the control group (p<0.005). The numbers of mast cells in the control group were inclined to increase significantly according to the mammary tumor development (p<0.005). In contrast, the mast cells were fewer significantly in the compound 48/80-treated group and Rompun-treated group than in the control group (p<0.005). The numbers of mast cells in the compound 48/80-treated group and Rompun-treated group were inclined to reduce significantly according to the stages of the mammary carcinoma growth in contrast to the control group respectively. The ultrastructural morphologies of mast cells at 30 minutes after Rompun injection were appeared many normal granules in the cytoplasm, but many normal and degranulated granules were scattered along the cell membrane. And at 1 hour after Rompun injection mast cell granules were disappeared nearly or rarely seen. many long cytoplasmic projections were folded back to adhere to their own surface membrane. and mast cells resulted in a reduced size of these cells. Otherwise. compound 48/80 caused extensive degranulation of mast cells by disrupting cell membrane. but mast cell degranulation by Rompun was observed exocytosis of granules through a channel. From the above results. it is concluded that the Rompun may give rise to the dealth of animals as a shock caused by mast cell degranulation.

• 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..

• Applied Microscopy
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• v.13 no.1
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• pp.41-47
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• 1983

A Scanning electron microscope which can obtain additional information not readily available with either the light or transmission electron microscope was used to study the mast cell shape and its granules in normal mammal tissue(rat mesentery, stomach and mouse stomach) by fretting cut using liquid nitrogen. The results showed that rat mesentery and mouse stomach mast cell surfaces had no ridges and microvilli, but revealed several microvilli projecting into the surrounding connective tissue in the rat stomach mast cell. The shape of the mast cell varied from discoid(in the rat mesenteric mast cell) to ellipsoid (rat and mouse stomach), ranging from 7.5 to $10{\mu}m$ in diameter. The shape of the nucleus was ellipsoid and nucleic membrane was adherent to the outer surface of the granules. The granules, approximately 0.2 to $0.9{\mu}m$ in diameter, were various shapes. Frequently, rounded protrusions of cytoplasmic granules could be discerned under the cell membrane. Many small granules were seen in the cytoplasm.

• Advances in Traditional Medicine
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• v.10 no.3
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• pp.200-207
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• 2010

The fruits of Piper cubeba L. are used traditionally to treat respiratory disorders in Indonesia. In order to determine the compounds responsible for this activity, the fruits were extracted with nhexane followed by ethanol to give n-hexane and ethanol extracts. Based on tracheospasmolytic assay on these two extracts, the n-hexane extract was more active to inhibit trachea contraction than that of ethanol extract. Upon bioassay guided isolation of the n-hexane extract, a tracheospasmolytic active compound was isolated and identified as dihydrocubebin [(3,4),(3',4')-bis-methylenedioxy-9,9'dihydroxylignan] $(\underline{1})$. Compound $\underline{1}$ was tested further for its ability to inhibit histamine released from mast cells, using rat basophilic leukemia (RBL-2H3) cell line and rat peritoneal mast cells RPMCs) as models; and $DNP_{24}$-BSA, thapsigargin, ionomycin, compound 48/80 and PMA were used as inducers for histamine released from mast cell. The test result showed that $\underline{1}$ inhibited histamine release from RBL-2H3 cells induced by $DNP_{24}$-BSA, thapsigargin and ionomycin. In addition, $\underline{1}$ suppressed histamine release from RPMC induced by either thapsigargin or ionomycin. However, $\underline{1}$ did not inhibit histamine release from RPMC induced by either compound 48/80 or combination PMA-sub optimum dose of ionomycin. Therefore, it was concluded that the inhibitory effects of $\underline{1}$ on the histamine released from mast cells may involve mechanisms related to intracellular $Ca^{2+}$ signaling events or downstream processes of intracellular $Ca^{2+}$ signaling in mast cells.