Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0220723 (PCA)
 4,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

PRD-92-Ea [5,5-Dimethyl-11-oxo-5H, 11H-(2) benzopyrano (4,3-g) (1) benzopyran-9-carboxylic acid ethanolamine], was an active antiallergic compound in rat and monkey experimental models of immediate hypersensitivity. It inhibited, in a dose-dependent manner, the rat PCA reaction after both intravenous and oral administration. It also inhibited the degranulation of rat peritoneal mast cells after antigenic challenge. PRD-92-Ea was also active in preventing bronchoconstriction in Ascaris-sensitive Rhesus monkeys after intravenous, topical and oral administration. Using chopped monkey tissues, it was found that PRD-92-Ea prevented histamine release from the respiratory mast cells, but not from the cutaneous mast cells. No reason for this dichotomy of effect is known. PRD-92-Ea showed antagonistic activity against the allergic mediators released from mast cells. In order of decreasing potency it was active against SRS-A (monkey lung), PGF2alpha, PGE2, serotonin, bradykinin and histamine. Apart from its antiallergic effects PRD-92-Ea had no other significant pharmacological activity.
 ...
PMID:Pharmacologic profile of a new antiallergic compound PRD-92-Ea. 7 14

Anaphylactic release of slow-reacting substance of anaphylaxis (SRS-A) from chopped guinea pig lung was studied. The antibodies mediating the anaphylactic reaction were classified as IgG antibodies by PCA technique. Isoprenaline was found to inhibit the release of SRS-A in the concentration range 10-8-10-6M, while the beta2-selective agonist terbutaline showed inhibition in the concentration range 10-6-10-5M. The beta1-selective beta-agonist tazolol was ineffective when tested in the concentration range 10-7-10-5M. The rank order of inhibitory potency of the compounds on SRS-A release agree with that for histamine release.
 ...
PMID:Release of slow-reacting substance from anaphylactic lung tissue and its modification by beta-sympathomimetics. 43 10

We studied the effects of OKY-046 on type I allergic reactions. OKY-046 (100 mg/kg) given orally suppressed antigen-induced bronchoconstriction and TXB2 generation in broncho alveolar lavage fluid in rats passively sensitized with anti-DNP-As monoclonal IgE. At the dose of 30 mg/kg given intraduodenally, it also inhibited antigen-induced bronchoconstriction in guinea pigs passively sensitized with anti DNP-As serum and actively sensitized with ovalbumin. However, aspirin (30 mg/kg) didn't suppressed them significantly. Azelastine (10 mg/kg) inhibited bronchoconstriction in passively sensitized rats and actively sensitized guinea pigs. In 48 hour homologous PCA reactions of rats and mice, oral administration of OKY-046 (300 mg/kg) and tranilast (100 mg/kg) suppressed the extravasated dye in the skin. OKY-046 decreased histamine release from passively sensitized rat peritoneal exudate cells. There was no effect of OKY-046 on SRS-A and leukotriene release from actively sensitized guinea pig lungs and passively sensitized rats. In conclusion, we think that OKY-046 should be an useful asthmatic drug or anti-allergic drug by oral administration.
 ...
PMID:[Anti-allergic effects of (E)-3-[p-(1H-imidazol-1-lylmethyl) phenyl]-2-propenoic acid (OKY-046), a specific thromboxane (TX) A2 synthetase inhibitor: effects on type I allergic reactions]. 169 6

Astemizole (0.5-5 mg/kg, p.o.) dose-dependently inhibited heterologous and homologous PCA reactions in rats at ID50 values of 1.48 mg/kg and 2.37 mg/kg, respectively. The inhibitory effect of astemizole on heterologous PCA was most remarkable when this compound was given p.o. 2 h prior to antigen challenge. Astemizole (0.1-5 mg/kg, p.o.) dose-dependently inhibited experimentally-induced asthma in guinea pigs at an ID50 of 0.86 mg/kg. Ex vivo, astemizole (0.5-5 mg/kg, p.o.) inhibited antigen-induced histamine release from lung pieces of sensitized guinea pigs. In in vitro experiments, the drug dose-dependently inhibited antigen-induced histamine and SRS-A releases from guinea pig lung pieces at concentrations of 0.05-10 microM. Furthermore, astemizole (0.1-10 microM) inhibited the histamine release induced by compound 48/80 and antigen-antibody reaction from rat peritoneal mast cells, and at 0.1-500 nM inhibited both leukotriene C4- and platelet-activating factor (PAF)-induced contraction of isolated guinea pig trachea at submicromolar concentrations. Astemizole not only inhibited 45Ca uptake into rat mast cells but also prevented the Ca2+ release from the intracellular Ca store induced by compound 48/80, although this compound did not affect the histamine release from permeabilized mast cells induced by Ca2+. Our results suggest that one of the antiallergic mechanisms of astemizole may be an inhibition of signal transduction from the mast cell membrane to the intracellular systems.
 ...
PMID:Antiallergic effects of astemizole on immediate type hypersensitivity reactions. 170 34

Amoxanox inhibited immunologically stimulated and LTD4-induced bronchoconstriction in laboratory animals. Amoxanox, like DSCG, inhibited rat IgE-mediated PCA and histamine release from rat peritoneal mast cells, and suppressed immunologically stimulated or calcium ionophore A23187-induced SRS-A generation in rat peritoneal cavity and guinea pig lung fragments. This compound also reduced the contractile response of guinea pig lung parenchymal and ileal strips to LTD4, but did not significantly affect the response of the ileum to either histamine or acetylcholine. Therefore, the antiallergic action of amoxanox seems to be associated with inhibition of chemical mediator release and antagonistic activity on SRS-A.
 ...
PMID:Mechanism of the action of amoxanox (AA-673), an orally active antiallergic agent. 241 69

The effects of a new anti-allergic agent, MY-5116: isoamyl 5,6-dihydro-7,8-dimethyl-4,5-dioxo-4H-pyrano [3,2-c] quinoline-2-carboxylate, and its main metabolite, MY-1250: 5,6-dihydro-7,8-dimethyl-4,5-dioxo-4H-pyrano [3,2-c] quinoline-2-carboxylic acid, on 48 hr homologous PCA (PCA) in rats and the release of histamine and SRS from rat peritoneal exudate cells (PEC) induced by IgE antibody in comparison with other anti-allergic agents were investigated. Also, the effects of MY-5116 and MY-1250 on antagonistic action against histamine and LTD4 were studied. MY-5116, tranilast and ketotifen inhibited PCA at oral doses of more than 3 mg/kg, 300 mg/kg and 0.3 mg/kg, respectively. MY-1250, DSCG and tranilast inhibited significantly the release of histamine from PEC induced by the antigen-antibody reaction in a dose-dependent manner, and the values of IC50 were 4.9 X 10(-8), 4.8 X 10(-6) and 4.6 X 10(-6) g/ml, respectively. Ketotifen inhibited significantly the release of histamine at a concentration of 10(-5) g/ml, but it accelerated significantly the release of histamine from PEC at a concentration of 10(-4) g/ml. MY-1250 and tranilast suppressed the release of SRS from PEC induced by the antigen-antibody reaction. The values of IC50 of MY-1250 and tranilast were 1.5 X 10(-6) and 2.1 X 10(-6) g/ml, respectively. MY-1250 suppressed slightly the release of SRS from PEC induced by A23187. MY-5116 showed no effect on the increase of vascular permeability induced by histamine, bradykinin and serotonin in rats.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Inhibitory effect on the release of mediators from rat peritoneal exudate cells and the antagonistic effect against mediators of MY-5116 and other anti-allergic agents]. 243 83

Terfenadine dose-dependently inhibited rat homologous PCA (2.5-10 mg/kg, p.o.) and experimentally-induced asthma in guinea pigs (0.5-5 mg/kg, p.o.). Similarly, metabolites I and II dose-dependently inhibited experimentally-induced asthma but their respective potencies were approximately 1/2 and 1/15th that of terfenadine. These results suggest that the metabolites contribute to the antiallergic effects of terfenadine. In ex vivo, terfenadine (5-20 mg/kg, p.o.) also inhibited the release of both antigen-induced histamine and SRS-A from sensitized guinea pig lung samples and that of histamine from rat peritoneal mast cells. Terfenadine dose-dependently increased the cAMP content in rat mast cells and in the lungs; in the latter, the augmented cAMP is associated with an increase in adenylate cyclase activity, but not with the inhibition of phosphodiesterase activity. The above evidence indicates that the inhibitory effects of terfenadine on mediator release from mast cells are in some way related to its antiallergic effects, and that an elevated cAMP content may be effective to enhance mediator release inhibition.
 ...
PMID:Antiallergic effects of terfenadine on immediate type hypersensitivity reactions. 244 87

IgG1, antibody-mediated homologous passive cutaneous anaphylaxis at 1.5 h (1.5-hour PCA) was elicited in the ears of mice and the effects of different drugs were studied. The reaction, as measured by the amount of extravasated dye, was inhibited by antihistamines, antiserotonins, cyclic AMP-elevating agents, tranilast and ketotifen, but not by an SRS-A antagonist (FLP 55712), lipoxygenase inhibitors, cyclooxygenase inhibitors and disodium cromoglycate. These results suggest that the pharmacological profile of 1.5-hour PCA resembles that of 48-hour PCA mediated by IgE antibody in the mouse ear.
 ...
PMID:Effects of different drugs on passive cutaneous anaphylaxis elicited in the mouse ear at 1.5 hours. 245 88

The antiallergic activity of sodium 10-(2,3-dimethyl pentanamido)-4-oxo-4H-pyrimido [1,2-C] quinazoline-3-carboxylate-hydrate (FR50948) was studied and compared with the activities of sodium cromoglycate (SCG) and lodoxamide. FR50948 had inhibitory effects on type I and type III allergic reactions, but not on type II and IV allergic reactions. FR50948 also had weak inhibitory effects on inflammation (carrageenin paw edema and adjuvant arthritis) and SRS release from rat neutrophils, but no antagonistic effects to histamine and serotonin. The inhibitory effect of FR50948 on IgE-mediated type I allergic reactions was essentially the same as those of SCG and lodoxamide, because FR50948 inhibited the histamine release from rat peritoneal mast cells and had cross tachyphylaxis with SCG in the rat PCA test. However, FR50948, like lodoxamide, had a stronger activity than SCG and was effective by the oral route, unlike SCG which was effective only by the parenteral route. Furthermore, the inhibitory effects of FR50948 on type III reactions and inflammatory reactions were much more potent than those of SCG and equal to those of lodoxamide, and the effect on IgG-mediated PCA was stronger than that of either reference drug. These results suggest that FR50948 will be beneficial in clinical use.
 ...
PMID:Effects of FR50948, a new orally active antiallergic agent, in experimental allergic models. 245 28

Effect of Saiboku-to, which has been used for the therapy of bronchial asthma, on Type I hypersensitivity reactions was investigated. Forty eight-hr homologous PCA and antigen-induced histamine release in peritoneal cavities of rats passively sensitized with anti-DNP-As . IgE serum tended to be inhibited by the oral administration of Saiboku-to. On the other hand, 7-day homologous PCA in guinea pigs mediated by anti-BPO-BGG . IgE serum was significantly inhibited with 200 and 500 mg/kg of Saiboku-to given orally 2 hr prior to challenge. In experimentally caused asthma in guinea pigs, 200 mg/kg of Saiboku-to dramatically inhibited decreases in the rate and volume of respiration, and 500 mg/kg of the drug inhibited even an increase in the ratio of expiration time to inspiration time. The Schultz-Dale reaction in guinea pig tracheal muscle was significantly inhibited by the pretreatment with 10(-4) g/ml of Saiboku-to. The antigen-induced histamine release from sensitized guinea pig lung tissue was inhibited by 10(-6) to 10(-4) g/ml of Saiboku-to in a dose-dependent fashion, though the release of SRS-A was not affected. Saiboku-to did not show an antagonistic effect on allergic mediator-induced contraction in guinea pig ileum. From these results, it is considered that Saiboku-to shows an inhibitory activity on the Type I hypersensitivity reaction through the suppression of histamine release.
 ...
PMID:[Effect of Saiboku-to, a blended Chinese traditional medicine, on Type I hypersensitivity reactions, particularly on experimentally-caused asthma]. 258 Jul 64


1 2 Next >>