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)

To evaluate the acute effects of anti-asthmatic drugs in vitro, we examined the modulation of various anti-asthmatic drugs in therapeutic concentrations on PAF-induced human eosinophil chemotaxis. Aminophylline (20 micrograms/ml) and Isoproterenol (10 nM) inhibited PAF (3 X 10(-8) M)-induced eosinophil chemotaxis nearly 30%, whereas no inhibitory effects were observed by Dexamethasone (0.1 microM), Tranilast, Ketotifen or Azelastine. Aminophylline (20 micrograms/ml) also inhibited LTB4 (3 X 10(-8) M)-induced eosinophil chemotaxis nearly 30%, whereas it did not inhibit chemotaxis induced by zymosan (5 mg/ml)-activated serum. These results indicate that anti-asthmatic drugs except for aminophylline and isoproterenol, when used acutely in therapeutic concentrations, have no striking inhibitory effects on PAF-induced eosinophil chemotaxis. These results further suggest the possibility that there are different mechanisms in eosinophil chemotaxis induced by PAF, LTB4 or by C5a.
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PMID:[Effects of anti-asthmatic drugs on human eosinophil chemotaxis]. 164 17

We have previously reported that Tranilast, an anti-allergic agent, was rapidly taken into the cytoplasm of rat mast cells in vitro by means of light microscopic radioautography. The present study was performed at the electron microscopic level to elucidate the fine localization of this agent in the mast cells. The results revealed that the number of radioautographic silver grains in the cells increased by the incubation with 3H-labelled Tranilast for 0 to 60 min. and that many silver grains were localized on the specific granules, especially on the perigranular membranes. These results suggest that the mode of inhibitory action of mast cell degranulation by Tranilast is related to the specific localization of this agent on the perigranular membranes.
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PMID:Electron microscopic radioautographic study of the localization of an anti-allergic agent, Tranilast, in rat mast cells. 169 12

Tranilast (N-(3,4-dimethoxycinnamoyl)anthranilic acid), an anti-allergic drug, has been developed and used for the treatment of anaphylactic hypersensitivity such as bronchial asthma in Japan. Recently, many cases with eosinophilic cystitis associated with administration of this drug have been reported. In a series of studies to elucidate the pathoetiology of this unusual cystitis, the distribution of tranilast in urinary bladder of rats was investigated. Light microscopic radioautography using tritiated tranilast showed that this drug was localized specifically in the transitional epithelial cells of the mucosa and the endothelial cells of venous vessels for a fairly long time after an oral administration. These results should be taken into consideration in further studies of this drug-associated cystitis.
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PMID:Localization of the anti-allergic agent tranilast in the urinary bladder of rats as demonstrated by light microscopic radioautography. 169 75

A 38-year-old man with asthma developed eosinophilic polymyositis following the administration of Tranilast, an antiasthmatic agent. Low grade fever, erythematous rashes on the entire body, dysphagia, blood eosinophilia, elevations of serum creatine phosphokinase and myoglobin levels, and inverted T waves in the electrocardiogram were noted. A muscle biopsy showed focal degeneration of muscle fibers with an infiltrate of eosinophils and lymphocytes. A rechallenge with Tranilast resulted in erythema formation, blood eosinophilia, and elevations of some serum muscle enzymes and myoglobin levels. Tranilast was considered to be the causative agent. This is the first reported case of Tranilast-induced eosinophilic polymyositis.
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PMID:Eosinophilic polymyositis induced by tranilast. 169 28

The mechanism proposed to explain the antiasthmatic antiallergic action of Tranilast is the inhibition of chemical mediator release from mast cells and leukocytes as well as the antagonism of smooth muscle contracting activity of leukotrienes. It has been shown that this drug inhibits platelet aggregation induced "in vitro" by different stimuli. We investigated the effect of Tranilast on the release of thromboxane from guinea pig isolated lungs stimulated by the calcium ionophore A 23187 and the contraction of smooth muscle induced by this eicosanoid. Tranilast did not inhibit the release of arachidonic acid metabolites from the lungs but it prevented the contraction of the rat aorta induced by thromboxane released from lungs. Moreover, the drug antagonized the contraction of rat and rabbit isolated aortas stimulated by the thromboxane/endoperoxide mimetic U 46619. These effects might be mediated by a blockade of calcium uptake, since the drug was able to induce the relaxation of rabbit aortas previously contracted by potassium. Calcium ions are involved in the activation of mast cells, leukocytes, platelets and smooth muscle; therefore, the inhibition of calcium uptake might mediate the pharmacological properties of Tranilast.
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PMID:New approach to the mechanism of antiasthmatic action of Tranilast. 169 24

Patients with atopic dermatitis (AD) were treated with Tranilast, Interleukin-2 (IL-2) (production of T cells in vitro) and blood histamine values, before and after Tranilast therapy, were measured, and the following results were obtained: 1) Compared with healthy controls, the IL-2 producing ability of T cells in patients with AD was increased. 2) After Tranilast therapy, IL-2 production of T cells in AD decreased in quantity to the control level. 3) Skin lesion severities of AD were correlated with the quantity of IL-2 production of T cells. 4) Serum histamine levels were not significantly different between AD patients and healthy controls, before or after Tranilast therapy.
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PMID:Interleukin-2 production of T cells in atopic dermatitis. 169 92

Blood eosinophils obtained from 25 patients with bronchial asthma were reacted with anti-IgG or with normal rabbit serum as the control. Morphological changes were examined by light microscopy, scanning electron microscopy and transmission electron microscopy. Reactive eosinophils in morphology with anti-IgG (27.8 per cent) were significantly higher (p less than 0.001) than those with the control (1.2 per cent). We also examined the effects of ketotifen and tranilast, both of which have eosinophil chemotactic inhibitory functions, on the morphological changes. Ketotifen altered the morphological reactivation of eosinophils and the generation of leukotrienes induced by anti-IgG, and this inhibition occurred in a concentration-dependent manner. Tranilast had no effect on the morphology of eosinophils and the generation of leukotrienes. These results suggest that eosinophil IgG receptors may have a role in the pathogenesis of asthma and that ketotifen may prevent their reactivity and, thus, could be of potential use in the treatment of asthma.
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PMID:Effect of ketotifen on the reactivity of eosinophils with the incubation of anti-IgG. 169 28

Tranilast (N-5) as a mast-cell stabilizer is widely used in cases of bronchial asthma and nasal allergy. Some reports showed that N-5 is effective against keloids and ulcerative colitis. So, it is considered that N-5 inhibits cell-mediated immunity. N-5 inhibited BCG-CWS-stimulated lymphocyte proliferation which was proved to be mainly operated by OKT4 positive T cells. Production of the lymphokine from BCG-CWS-stimulated lymphocytes was suppressed by the addition of N-5. Thus, it is demonstrated that N-5 inhibits delayed type hypersensitivity in vitro.
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PMID:[Effect of tranilast (N-5) on cellular immunity--delayed type hypersensitivity]. 171 10

It has been well known that the number of mast cells increases during the development of fibrosis in various tissues including the lung. However, the role of mast cells in fibrosis still remains obscure. In the present paper, we evidenced that pulmonary fibrosis could be induced in genetically mast cell-deficient WBB6F1-W/Wv mice as well as WBB6F1-(+/+) mice having mast cells normally by the treatment with bleomycin (BLM, 5 mg/kg, i.v., 10 days), and there was not much difference in the histological changes of lungs between the two strains. An increase in the hydroxyproline content of the lung of WBB6F1-W/Wv mice was rather higher than that of WBB6F1-(+/+) mice. Previously, we reported that tranilast, an antiallergic drug inhibiting chemical mediator release from mast cells, suppressed the development of BLM-induced pulmonary fibrosis in ICR mice, suggesting the possibility that mast cells play certain roles in fibrosis. However, it was evidenced in the present report that tranilast suppressed BLM-induced fibrosis in WBB6F1-W/Wv mice. Tranilast neither suppressed the cytotoxic activity of BLM against KB cells and L-929 cells in vitro, nor inhibited the antitumor activity of BLM against Sarcoma-180 transplanted subcutaneously into ICR mice. Tranilast may act through suppressing BLM-induced activation of lymphoid cells including macrophage and neutrophil. These results indicate an inconsequential role of mast cells in the development of fibrosis. Increases in the number of mast cells and in histamine content of the lung, which were widely reported in the lungs of BLM-treated mice, may be the result of fibrosis.
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PMID:Bleomycin-induced pulmonary fibrosis in genetically mast cell-deficient WBB6F1-W/Wv mice and mechanism of the suppressive effect of tranilast, an antiallergic drug inhibiting mediator release from mast cells, on fibrosis. 171 9

The effect of tranilast, an inhibitor for IgE-mediated mediator release from mast cells, on plasma extravasation induced by the intradermal injection of substance P in rats was examined. Tranilast (100 mg/kg, intraperitoneally) decreased plasma extravasation induced by substance P (10(-7)-10(-5) M). Tranilast decreased plasma extravasation induced by the amino-terminal peptide substance P1-9 (10(-6)-10(-4) M), which is active for rat mast cells, but not by the carboxy-terminal peptide substance P6-11 (10(-6)-10(-4) M), which is inactive for the mast cells. Therefore, tranilast prevents substance P-induced plasma extravasation most likely by inhibiting mast cell degranulation.
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PMID:Inhibitory effect of tranilast on substance P-induced plasma extravasation in rat skin. 172 11


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