Pharmacological Characterization of Mouse Ear PCA

Inagaki, Nobuya; Goto, Shoichi; Nagai, Hiroichi; Akihide, Koda

doi:10.1159/000233873

Cited by 27 publications

(28 citation statements)

References 13 publications

(18 reference statements)

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“…In animal experiments, DSCG is known to be ineffec tive in guinea pigs and mice (18)(19)(20). In this study, DSCG had no effect on PCA in guinea pigs, anaphylactic hista mine release from guinea pig lung fragments or anaphylac tic release of pLTs from guinea pig lung fragments and mouse cultured mast cells.…”

Section: Discussionmentioning

confidence: 44%

Effects of Quinotolast, a New Orally Active Antiallergic Drug, on Experimental Allergic Models

Kobayashi

Hiroi

Kishi

et al. 1993

Japanese Journal of Pharmacology

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ABSTRACT-The effects of a new antiallergic drug, quinotolast [sodium 5-(4-oxo-1-phenoxy-4H quinolizine-3-carboxamido)tetrazolate monohydrate], were studied and compared with those of tranilast, amlexanox, pemirolast, repirinast and disodium cromoglycate (DSCG) in experimental allergic models. Quinotolast potently inhibited such type I allergic reactions as passive cutaneous anaphylaxis (PCA) and anaphylactic bronchoconstriction in rats by both intravenous and oral dosing. All of these effects were stronger than those of the reference drugs tested. Quinotolast inhibited histamine release from rat peritoneal cells, but it had no antagonistic effect on histamine-, serotonin-, platelet activating factor or bradykinin-induced cutaneous reactions in rats. Moreover, it was clearly demonstrated that quinotolast and DSCG had a cross tachyphylaxis to inhibit PCA in rats, suggesting that these drugs, at least in part, share the same mechanism of action. Furthermore, quinotolast potently inhibited PCA in guinea pigs in which DSCG and other reference drugs showed poor inhibitory activity. Quinotolast also showed stronger inhibi tory effects on histamine and peptide leukotrienes release from guinea pig lung fragments or mouse cultured mast cells than the other drugs tested. Thus, the effect of quinotolast on type I allergic reaction would seem to be based on an inhibition of mediator release from inflammatory cells including mast cells. The results suggest that quinotolast will be beneficial in the treatment of type I allergy-related diseases.

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Section: Discussionmentioning

confidence: 44%

Effects of Quinotolast, a New Orally Active Antiallergic Drug, on Experimental Allergic Models

Kobayashi

Hiroi

Kishi

et al. 1993

Japanese Journal of Pharmacology

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“…This may be related to the fact that both immunizing procedures resulted in the production of both IgE and IgG1 antibodies responsible for ACA. We reported previously, however, that mouse ear PCA mediated by both IgE and IgG1 antibodies are inhib ited similarly by these drugs (16,20).…”

Section: Discussionmentioning

confidence: 89%

“…According to these re ports, we established a method for PCA in the mouse ear by assessing the amount of extravasated dye (15) and characterized it pharmacologically and immunologi cally (16)(17)(18)(19)(20)(21)(22)(23). However, although passive sensitization provides a simple model that is suitable for analyzing the mechanisms involved in both allergic reactions and drug action, active sensitization is also important for studying allergic diseases, because allergic diseases are caused by active sensitization.…”

mentioning

confidence: 99%

Active Cutaneous Anaphylaxis (ACA) in the Mouse Ear

Inagaki

Miura

Nagai

et al. 1992

Japanese Journal of Pharmacology

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ABSTRACT-Active cutaneous anaphylaxis (ACA) was studied in the ear of female BALB/c mice. Mice were immunized with ovalbumin in the presence of aluminium hydroxide gel or complete Freund's adjuvant (CFA). Two weeks after the immunization, ACA was elicited in the mouse ear by injecting 10,ul of antigen solution intradermally into the ear lobe. ACA was assessed by the amount of extravasated dye, which was given intravenously just after the antigen injection. Antiallergic drugs (tra nilast, ketotifen and azelastine), antihistamines (chlorpheniramine, diphenhydramine and mequitazine), fl-stimulants (isoproterenol and salbutamol), theophylline and glucocorticoids (hydrocortisone, predni solone and dexamethasone) inhibited the reaction significantly. These drugs inhibited both ACA in mice immunized with alum-precipitated antigen and ACA in mice injected with CFA-emulsified antigen similarly. ACA in the mouse ear might be a useful tool for studying drugs for allergy.Keywords: Active cutaneous anaphylaxis, Ear (mouse), Antiallergic drug, IgE antibody, IgG1 antibody Passive cutaneous anaphylaxis (PCA) (1, 2) is a use ful experimental model for studying drugs for allergy (3 6). The rat has been the most useful species for this purpose and the reaction is assessed by measuring the amount of extravasated dye (7,8). On the other hand, the mouse is the most established experimental animal and there are many strains of mice with unique im munological characteristics (9-12).Furthermore, Feinberg (13) reported the suitability of mouse ear for induction of PCA, and Prouvost-Danon and Binaghi (14) demonstrated that mouse ear had higher reactivity for PCA than mouse dorsal skin. According to these re ports, we established a method for PCA in the mouse ear by assessing the amount of extravasated dye (15) and characterized it pharmacologically and immunologi cally (16-23). However, although passive sensitization provides a simple model that is suitable for analyzing the mechanisms involved in both allergic reactions and drug action, active sensitization is also important for studying allergic diseases, because allergic diseases are caused by active sensitization. In the present study, therefore, we applied the technique of mouse ear PCA to active cutaneous anaphylaxis (ACA) elicited in female BALB/c mice, and examined the effect of drugs which are used for allergic diseases on the ACA. MATERIALS AND METHODS MiceFemale BALB/c mice were used for ACA and male ddY mice were used for titration of serum antibodies. Both mice were purchased from Japan SLC, Inc. (Hamamatsu, Japan). Antigen and adjuvantsOvalbumin (OA, 5 times crystalized) was purchased from Seikagaku Kogyo Co., Ltd. (Tokyo, Japan). As adjuvants, aluminium hydroxide gel (alum) and com plete Freund's adjuvant (CFA) were used. Alum was prepared according to the method of Levine and Vaz (24), and CFA was obtained from Nacalai Tesque, Inc. (Kyoto, Japan). ACATen-weeks-old female BALB/c mice were immunized with OA in the presence of an adjuvant. To induce IgE antibody mainly, 1,ug...

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“…Mouse ear passive cutaneous anaphylaxis was induced by the method of Inagaki et al (16). Briefly, 10,ul of 50-fold diluted mouse serum containing anti-dinitrophenylated asca ris (DNP-As) IgE antibody was injected into both ears of ddY mice.…”

Section: Mouse Ear Passive Cutaneous Anaphylaxismentioning

confidence: 99%

“…Thirty minutes after the challenge, mice were sacrificed by cervical dislocation and both ears were removed to measure the amount of extravasated dye. The amount of dye was measured according to the previously described method (16). Briefly, a pair of ears was dissolved, overnight, in 0.7 ml of 1 N sodium hydroxide solution at 37°C, and 9.3 ml of a mixture of 0.6 N H3PO4 solution and ace tone (5 : 13) was then added.…”

Section: Mouse Ear Passive Cutaneous Anaphylaxismentioning

confidence: 99%

Effect of Three Novel K+ Channel Openers, Cromakalim, Pinacidil and Nicorandil on Allergic Reaction and Experimental Asthma.

et al. 1991

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ABSTRACT-The anti-allergic and anti-asthmatic activities of three potassium (K+) channel openers, cromakalim, pinacidil, and nicorandil, were investigated. 1) Forty eight-hour homologous passive cutaneous anaphylaxis (PCA) in mice was not affected by cromakalim, pinacidil, or nicorandil. Ketotifen significantly inhibited the reaction. 2) Antigen-induced histamine release from sensitized guinea pig lung tissue was not affected by cromakalim, pinacidil or nicorandil (except for 10-4 M nicorandil). Salbu tamol inhibited the release of histamine. 3) Histamine, serotonin and LTC4-induced vasculitis in rat back skin was not affected by any of these three K+ channel openers. 4) Antigen-induced constriction of isolated sensitized guinea pig tracheal muscle was relaxed by each of the K+ channel openers. 5) Constrictions of isolated guinea pig tracheal muscle caused by high potassium, histamine, LTC4, or U-46619 were clearly relaxed by each of the three K+ channel openers. 6) Increases of airway resistance caused by histamine, LTD4, or U-46619 in guinea pigs in vivo were inhibited by admin istration of each of the three K+ channel openers. 7) Experimental asthma caused by the IgE antibody and antigen system in guinea pigs was inhibited by each of the three K+ channel openers.

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Pharmacological Characterization of Mouse Ear PCA

Cited by 27 publications

References 13 publications

Effects of Quinotolast, a New Orally Active Antiallergic Drug, on Experimental Allergic Models

Effects of Quinotolast, a New Orally Active Antiallergic Drug, on Experimental Allergic Models

Active Cutaneous Anaphylaxis (ACA) in the Mouse Ear

Effect of Three Novel K+ Channel Openers, Cromakalim, Pinacidil and Nicorandil on Allergic Reaction and Experimental Asthma.

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