Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D02027 (Tranilast)
 205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental studies have shown that N(3',4'-dimethoxycinnamoyl) anthranilic acid (Tranilast) inhibits reaginic antibody-mediated hypersensitivity reactions, and it has been demonstrated to be an effective drug for patients with bronchial asthma. On the other hand, from the nature of the cellular infiltrate seen in eczematous lesions, it appears that some form of cell-mediated immunity may be involved in addition to IgE-mediated immunity in the pathogenesis of atopic dermatitis (AD). Moreover, we have previously reported that the proliferative responses of peripheral blood mononuclear cells (PBMCs) to ovalbumin (OA) or bovine serum albumin (BSA) in children with AD who are sensitive to hen's egg or cow's milk were significantly higher than those of healthy children and hen's egg or cow's milk sensitive children with immediate symptoms. In this study, we have showed that the proliferative responses of PBMCs to OA were dose-dependently inhibited by Tranilast on patients with AD. The responding cells to OA were shown, through separation experiments, to be T cells, and the proliferative responses of T cells to OA were also dose-dependently inhibited by Tranilast. Moreover, the inhibition was thought to occur at the initial stage of the proliferative reactions. These results suggest that Tranilast can be clinically applied to patients with AD.
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PMID:Inhibition of proliferative responses of lymphocytes to food antigens by an anti-allergic drug, N(3',4'-dimethoxycinnamoyl) anthranilic acid (Tranilast) in children with atopic dermatitis. 137 91

Guinea pigs were passively sensitized by sera containing antidinitrophenyl reaginic antibody and specifically challenged by dinitrophenyl-bovine serum albumin injected through the stylomastoid foramen. Nystagmus, head deviation, negative summating potentials on electrocochleography, and an increase of threshold and wave I peak latency on auditory brain stem response testing were observed after local challenge. These physiologic changes were reversible and resolved within several days. We also used Tranilast before the specific challenge. It is a blocking agent of chemical mediator release from mast cells. Negative summating potentials and head deviation were not observed after the use of this agent. In the animals that showed physiologic changes, we observed endolymphatic hydrops, mast cell degranulation, and eosinophil infiltration histologically in the challenged side of the inner ear. These results suggest that the physiologic and histologic changes provoked in the inner ear of the sensitized animals may have been induced by type I allergy.
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PMID:Type I allergy in the inner ear of the guinea pig. 138 14

Slow reacting substance of anaphylaxis (SRS-A) and slow reacting substance (SRS) were released from actively sensitized guinea-pig lung with bovine serum albumin and from rat peritoneal exudate cells with ionophore A23187, respectively. FPL55712 markedly inhibited the contraction induced by SRS-A and SRS in guinea-pig ileum which was treated with atropine (10(-7) g/ml), mepyramine (10(-6) g/ml), and cyproheptadine (10(-7) g/ml). Tranilast and isoproterenol markedly suppressed the release of SRS-A in a dose-dependent manner; the concentrations of these drugs that gave 50% inhibition (IC50) were 1.1 X 10(-4)M and 8.3 X 10(-9)M, respectively. Although the inhibitory effect of tranilast (10(-3)M) was not affected in the presence of propranolol (3 X 10(-6)M), the inhibitory effect of isoproterenol was greatly diminished by propranolol. Also, tranilast markedly suppressed the release of SRS in a dose-dependent manner, its IC50 being 6.4 X 10(-5)M. However isoproterenol slightly inhibited the release of SRS. Disodium cromoglycate did not suppressed the release of SRS-A at all, and it suppressed SRS release a little. Tranilast inhibited the contraction induced by leukotriene C4 (0.5 ng/ml) and D4 (1 ng/ml) in guinea-pig trachea in a dose-dependent manner; the IC50 values were 2.2 X 10(-4)M and 2.0 X 10(-4)M, respectively, for these inhibitions. These results suggest that the inhibition of SRS-A release and SRS-A-induced contraction of smooth muscle by tranilast participates in the anti-asthmatic effect of tranilast, and its inhibitory mechanism is different from that of isoproterenol.
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PMID:[Effect of tranilast on the release of slow reacting substance of anaphylaxis (SRS-A) and contraction of the smooth muscle]. 619 82

Time course studies of electrocochleography and the auditory brain stem response were performed in guinea pigs that were passively sensitized by sera containing antidinitrophenyl reaginic antibody and specifically challenged by dinitrophenyl-bovine serum albumin injected through the stylomastoid foramen. A negative summating potential on electrocochleography was observed from 12 to 48 hours, but not at 72 hours, after the specific challenge. A threshold increase on the auditory brain stem response was observed 15 minutes after the specific challenge; the threshold recovered to the prechallenge level within 7 days. Further, we used Tranilast, a blocking agent of chemical mediator release from mast cells, before the specific challenge. A negative summating potential and head deviation were not observed after the use of this agent. These results suggest that the auditory change provoked in the inner ear of the sensitized guinea pig may have been induced by type I allergy.
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PMID:Audiological study in guinea pigs with type I allergy induced in the inner ear. 768 18