• Advances in Traditional Medicine
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• v.8 no.1
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• pp.24-31
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• 2008

In the present investigation, we studied the effect of alcoholic extract of Moringa oleifera (M. oleifera) seed kernels on various experimental models of bronchial asthma. Significant (P < 0. 05) increase in preconvulsion time was observed due to pretreatment with M. oleifera when the guinea pigs were exposed to either acetylcholine (Ach) or histamine aerosol. This bronchodilating effect of M. oleifera was comparable to ketotifen fumarate. Spasmolytic effect of M. oleifera was also observed by dose dependent inhibition of ideal contractions induced by Ach, 5HT, histamine and $BaCl_2$. Alcoholic extract of M. oleifera produced significant dose dependent protection by egg albumin and compound 48/80 induced mast cell degranulation. Pretreatment with alcoholic extract of M. oleifera also decreased carrageenan induced rat paw edema, which was comparable to that of standard diclofenac sodium. Minimum inhibitory concentration for alcoholic extract of M. oleifera was low as compared to cold-water extract and hot water extract when antimicrobial activity was tested against various respiratory pathogens like Escherichia coli (E. coli), Staphylococus aureus (S. aureus) and pseudomonas aeruginosa (P. aeruginosa). Our data suggest that antiasthmatic activity of M. oleifera seed kernels may be due to its bronchodilator, anti-inflammatory, mast cell stabilization and antimicrobial activity.

• Journal of Life Science
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• v.22 no.5
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• pp.595-599
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• 2012

Allergic response is associated with mast cells, through the release of arachidonic acid, proinflammatory cytokines, and histamine. We investigated the effect of Platycodon grandiflorum including platycodin D (PG-Platycodin D) on allergic responses in an animal model and on mast cell degranulation. PG-Platycodin D suppressed the release of ${\beta}$-hexosaminidase, a type of marker associated with degranulation. PG-Platycodin D efficiently inhibited the passive cutaneous anaphylaxis (PCA) reaction in ICR mice. In addition, molecular analysis demonstrated that PG-Platycodin D inhibited mRNA expression of both IL-3. These results suggest that PG-Platycodin D can inhibit mast cell degranulation through the inhibition of IL-3 mRNA expression, and that PG-Platycodin D may potentially serve as an anti-allergic agent.

• Journal of Ginseng Research
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• v.20 no.1
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• pp.1-6
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• 1996

Effects of Panax ginseng on allergic reactions were studied uslng various in vivo and in vitro experimental models such as 48-hr passive cutaneous anaphylaxis, mediators-induced skin reactions, histamine release from rat peritoneal mast cells, hexosaminidase release from RBL-2H3 cells, and lipoxygenase assay . In all of anti-allergic experiments we conducted, ginseng components (50% ethanol extract or ginseng total saponin or ginsenosides) extracted from Korean red ginseng, did not show significant anti-allergic actions. In 48-hr passive cutaneous anaphylaxis and mediators-induced skin reactions, 50% ethanol extract did not suppress hypersensitivity reactions. Total saponin, 50% ethanol extract, and 8 major ginsenosides did not show inhibitory effects on lipoxygeanse activity. Ginseng total saponin did not inhibit histamine release from rat peritoneal mast cells. All of the ginseng components mentioned above were also tested on RBL-2H3 cells, but none of them inhibited hexosaminidase release from this cell line. These results suggest that Panax ginseng does not have effects on allergic reactions at the level of 50% ethanol extract or total saponin used. All of 8 major saponin components tested ($Rb_1$, $Rb_2$, Rc, Rd, Re, Rf, $Rg_1$, $Rg_2$), did not inhibit lipoxygenase activity and degranulation events.

• Biomolecules & Therapeutics
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• v.27 no.3
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• pp.311-317
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• 2019

Mast cells are the most prominent effector cells of Type 1 hypersensitivity immune responses. CYC116 [4-(2-amino-4-methyl-1,3-thiazol-5-yl)-N-[4-(morpholin-4-yl)phenyl] pyrimidin-2-amine] is under development to be used as an anti-cancer drug, but the inhibitory effects of CYC116 on the activation of mast cells and related allergy diseases have not reported as of yet. In this study, we demonstrated, for the first time, that CYC116 inhibited the degranulation of mast cells by antigen stimulation ($IC_{50}$, ${\sim}1.42{\mu}M$). CYC116 also inhibited the secretion of pro-inflammatory cytokines including TNF-${\alpha}$ ($IC_{50}$, ${\sim}1.10{\mu}M$), and IL-6 ($IC_{50}$, ${\sim}1.24{\mu}M$). CYC116 inhibited the mast cell-mediated allergic responses, passive cutaneous anaphylaxis (ED50, ~22.5 mg/kg), and passive systemic anaphylaxis in a dose-dependent manner in laboratory experiments performed on mice. Specifically, CYC116 inhibited the activity of Fyn in mast cells and inhibited the activation of Syk and Syk-dependent signaling proteins including LAT, $PLC{\gamma}$, Akt, and MAP kinases. Our results suggest that CYC116 could be used as an alternative therapeutic medication for mast cell-mediated allergic disorders, such as atopic dermatitis and allergic rhinitis.

• YAKHAK HOEJI
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• v.34 no.5
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• pp.348-364
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• 1990

The activities of twenty-one flavonoids and their related compounds on the hypersensitivity reaction against various antigens were studied in vitro and in vivo. 1. Generally flavonoids inhibited significantly the homologous passive cutaneous anaphylaxis (PCA) induced by reaginic antibody as compared as anaphylaxis by compound 48/80-induced mast cell degranulation, and so more strongly active in the IgE-mediated anaphylaxis than non-IgE-mediated anaphylaxis. 2. Flavonids inhibited remarkably Arths reaction, hemolysin titer, delayed hypersensitivity, haemagglutinin titer, rosette forming cells and plague forming cells against sheep red blood cells, and so it exhibited that flavonoids inhibited type 2, 3 and 4 hypersensitivity. 3. Quercetin, kaempferol, hesperetin, disodium cromoglycate, malvin and baicalein were active dose-dependently in the all types of hypersensitivity. Fisetin, daidzein, morin, narigin, flavone, catechin, rutin, hesperidin, neophsperidin, apigenin and chrysin were significantly active in the various types of hypersensitivity, but apigenin, rutin and catechin were less active in the delayed hypersensitivity. Taxifolin was significantly active in PCA and histamine-induced anaphylaxis except other types of hypersensitivity. Rotenone and cyanin also inhibited all types of hypersensitivity, but they are toxic. 4. Based on these results from hypersensitivity, the following flavonoid structure-activity relationships became apparent. 1) Flavonoids with $C_{2-3}$ double bond in C-ring were more active than that of $C_{2-3}$ saturation. 2) Flavonoids with $C_4$ ketone group in C-ring were more active than abscence of them except catechin and malvin. 3) Flavonoids with benzene ring at positions 2 or 3 in C-ring exhibited same activities. 4) Flavonoids with opening of the C-ring does not abolish their activities. 5) The glycosylated flavonoids in position 3 or 7 was less active than their aglycone. 6) Flavonoids with the more hydroxy group in A and B-ring were more active. 7) Flavonoids with or without $C_3-OH$ did not change their activities.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1994.04a
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• pp.243-243
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• 1994

Although active systemic anaphylaxis and passive cutaneous anaphylaxis have been empolyed to study anaphylactic hypersensitivity, it is difficult and time-consuming to induce these reactions in experimental animals. In recent, Jun et al have found a simple method to induced anaphylactic hypersensitivity such as anaphylactic shock(AS) and cutaneous reaction(CR) using compound48/80. Cortex mori (Morus alba L.), the root bark of mulberry tree has been used as an antiphlogistic, diuretic, and expectorant in herbal medicine. The purpose of this study was to determine whether the methanol extract of Cortex mori could inhibit the compound 48/80-induced AS and CR. To induce AS, various doses of compound 48/80 (5, 7.5, 10, 15$\mu\textrm{g}$/gm B.W.) were injected intraperitoneally (i.p.) into ICR mice. The animals were pretreated by three injection(i.p.) of Cortex mori before compound 48/80 administration. Peripheral blood was collected from the right ventricle to estimate the level of serum histamine at 15 minutes after the injctin(i.p.) of various concentration of compound48/80. Mortility rate, mean death time and mesenteric mast cell degranulation rate were evaluated over a 72 hour period. To estimate the effect of Cortex mori on compound 48/80-induced cutaneous reaction, various doses of compound 48/80 with or without Cortex mori were injected intradermally(i.d.) into the shaved flank of Sprague-Dawley rats, and the blue cutaneous patchs induced by Evans'blue injection at the compound 48/80 alone and Cortex mori plus compound 48/80 injection sites were observed. As a Parameter of these reactions, the levels of histamine in the supernatant, calcium uptake and intracellular CAMP of RPMC were measured. supernatant, 1)compound 48/80-induced mortility rate, mean death time, mesenteric mast cell degranulation rate, and serum histamine level in ICR mice were significantly inhibited by pretreatment of Cortex mori, 2) cutaneous reaction inducd by compound48/80 was well developed in Sprague-Dawley rat, but Cortex mori inhibited the compound 48/80-induced blue patch formation remarkably, 3) the compound 48/80-induced degranulation, histamine release and calcium uptake of RPMC pretreated with Cortex mori were significantly inhibited, compared to those of control without Cortex mori pretreatment, and 4)the level of cAMP of RPMC was reduced bythe increased concentration of compound 48/80, pretreatment of Cortex mori not only inhibited the compound 48/80-induced reduction of CAMP but also significantly increased the level of cAMP naturally, from the above results, it is suggested that Cortex mori has an some substances with an ability to inhibits the compound 48/80-induced AS,CR, and mast cell activation.

• IMMUNE NETWORK
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• v.2 no.3
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• pp.158-165
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• 2002

Background: Toluene diisocyanate (TDI) can cause contact allergy and occupational asthma, but the mechanism underlying sensitization to this chemical compound remains controversal. Also the correlation of mast cell with contact hypersensitivity (CHS) and the role of mast cell in the TDI-induced CHS is unknown. This issue was investigated by administrating TDI on the skin of genetically mast cell-deficient WBB6F1/$J-Kit^{W}/Kit^{W-v}$ ($W/W^{V}$) and congenic normal WBB6F1/J-Kit+/+ (+/+) mice. Methods: To development of animal model of TDI-induced CHS and to investigate the correlation of mast cell with CHS and the role of mast cell in the TDI-induced CHS, $W/W^V$ and +/+ mice were sensitized with TDI on the back skin at day 1 and day 8, and then challenged with 1% TDI on the ear at day 15. At 1, 2, 4, 8, and 24 hours after 1% TDI challenge, the ear thicknesses were measured. It was investigated the histologic changes of dermis in the ear of $W/W^V$ and +/+ mice at 24 hours after 1% TDI challenge. Results: TDI induced a significant ear swelling response in $W/W^V$ and +/+ mice. TDI induced the significant infiltrations of polymorphonuclear leukocytes and eosinophils in $W/W^V$ and +/+ mice, but not of mast cells in normal mice. And TDI increased a characteristic extent of mast cell degranulation in normal mice. There were no significant differences in the ear swelling and the infiltrations of polymorphonuclear leukocytes and eosinophils of normal versus $W/W^V$ mice, either at baseline or after TDI-induced CHS. Conclusion: From the above results, TDI can be used as a murine CHS model, and the mast cells may not be essential in TDI-induced CHS.

• Journal of Life Science
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• v.19 no.10
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• pp.1444-1450
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• 2009

The number of patients with immune- mediated dermatitis such as contact dermatitis is increasing year by year. Allergic contact dermatitis is a complex phenomenon that involves resident epidermal cells, fibroblasts, and endothelial cells, as well as invading leukocytes that interact with each other under the control of a network of cytokines and lipid mediators. It is a cell-mediated immune reaction, which occurs after susceptible individuals are exposed to sensitizing chemicals, and characteristic eczematous reaction is seen at the point of contact with an allergen. In this study, we investigated the allergy prevention effects of quercetin on mast cell-mediated allergic inflammation in BALB/c mice. BALB/c mice were sensitized with 40 ${\mu}l$ of 1.5% picryl choloride (PCL) to the left and right ear each. Total serum IgE levels and histamine levels were measured by the sandwich ELISA method using mouse IgE, histamine measuring kit. For histopathological examination, paraffin sections were stained with hematoxylin and eosin(HE) or toluidine blue(TB). Ear swelling responses were much weaker in the high-dose group (100 mg/kg) than the control group (0 mg/kg). The number of mast cells showed a significant decrease in the high-dose group (100 mg/kg) compared to the control group (0 mg/kg). Degranulation of mast cells was also confirmed by Toluidine Blue (TB) staining method. Both total serum IgE and histamine levels were significantly decreased in the high-dose group (100 mg/kg) compared to other groups. These findings suggest a certain relationship between the elevation of IgE, histamine levels and the degranulation of mast cells. These results show that the pharmacological actions of quercetin indicate its potential activity for prevention of allergic inflammatory diseases through the down-regulation of mast cell activation.

• Journal of Mushroom
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• v.12 no.4
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• pp.324-329
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• 2014

For evaluating the anti-allergy activity of mushrooms, forty two mushroom extracts were studied their inhibitory activities on the IgE-mediated degranulation in rat basophilic leukemia cell line (RBL-2H3 cell). Effects of mushroom extracts on the release of interleukin-4 (IL-4) and beta-hexosaminidase, and the cell viability of the IgE-sensitized were measured. From the analysis, five mushroom extracts such as the water extract from Flammulina velutipes (Curt.:Fr.) Sing showed the suppressive activities on IL-4 release as 20%. Eight extracts including the water extract of Ganoserma lucidum showed the suppressive activities on ${\beta}$-hexosaminidase release as 20%. Almost all of the extracts stimulated the proliferation of RBL-2H3 cell. The water extracts of Flammulina velutipes and Phellinus linteus were examined against the inhibitory activity in the production of IL-4 and ${\beta}$-hexosaminidase. Additionally, the extracts from Ganoserma lucidum, Isaria japonica, Phellinus linteus and Pleurotus ostreatus inhibited dose-dependently on ${\beta}$-hexosaminidase production. In conclusion, the result suggests that the mushrooms with the potent inhibitory efficacies on the degranulation of the mast cell would be candidate resources for the anti-allergy resources, and thus need to study for their utilization.

• Korean Journal of Food Science and Technology
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• v.30 no.2
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• pp.468-471
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• 1998

Regarding the characterstics of allergic diseases, preventive and continuous treatment is desirable, and tea would be the one of the best functional food formula for it. Here we report the development of tea processing method for the leaves of Castnaea crenata. Two forms of Castnaea crenata leaf tea were prepared, non-fermented steaming tea and semi-fermented rolling tea. Anti-allergic actions of Castanea crenata leaf tea were asessed by testing their effects on the degranulation of mast cells. For this, hexosaminidase release (degranulation marker) from RBL-2H3 cells (mast cell line) was used. At the concentration of $300\;{\mu}g/mL$ of the water extract, the degranulation of RBL-2H3 cells were inhibited 50.4% and 35.4% by non-fermented steaming tea and semi-fermented rolling tea, respectively. These results suggest that the tea processing method we developed could provide a valuable resource for the treatment of allergic diseases.