calcimycin has been researched along with tranilast* in 7 studies
7 other study(ies) available for calcimycin and tranilast
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Inhibitory effects of azelastine and tranilast on leukotriene B4 and leukotriene C4 generation by rat colonic mucosa.
Anti-allergic drugs such as sodium cromoglycate are known to be effective for the treatment of ulcerative colitis (UC). Because leukotriene (LT) production is considered to play an important role in the pathophysiology of UC, we examined the effect of the anti-allergic drugs, azelastine and tranilast, and the 5-lipoxygenase inhibitor, AA861, on LTB4 and LTC4 production by isolated rat colonic mucosa treated with the calcium ionophore, A23187. Preincubation of colonic mucosa with AA861 (10(-4) M) or azelastine (10(-4) M) significantly reduced AA23187-induced LTB4 (p < 0.01 and p < 0.05, respectively) and LTC4 (p < 0.01) production. Pretreatment with tranilast (10(-3) M) also significantly reduced A23187-induced LTC4 production (p < 0.05). These findings suggest that azelastine and tranilast can inhibit LT production in colonic mucosa and may be beneficial in the treatment of patients with UC. Topics: Animals; Anti-Allergic Agents; Calcimycin; Colon; Intestinal Mucosa; Leukotriene B4; Leukotriene C4; Male; ortho-Aminobenzoates; Phthalazines; Rats; Rats, Wistar | 1995 |
Effect of azelastine on leukotriene synthesis in murine peritoneal cells and on thromboxane synthesis in human platelets.
Azelastine, a newly synthesized antiallergic agent, strikingly inhibited the production of leukotriene B4 and C4 (LTB4 and LTC4) in murine peritoneal cells which had been stimulated by calcium ionophore A23187. The 50% inhibitory concentrations (IC50) of the agent were approximately 1.0 x 10(-5) M. In addition, azelastine significantly inhibited also 5-lipoxygenase activity in peritoneal cells with an IC50 of 1.0 x 10(-5) M, but not on LTC4 synthetase, LTA4 hydrolase or phospholipase A2 activity. Furthermore, azelastine showed little effect on either 12-lipoxygenase activity or thromboxane synthesis in human platelets. These results suggest that at least the drug's antiallergic effects can be attributed to its inhibiting action of 5-lipoxygenase in regard to arachidonate metabolism. Topics: Animals; Blood Platelets; Calcimycin; Dose-Response Relationship, Drug; Epoxide Hydrolases; Glutathione Transferase; Hydroxyeicosatetraenoic Acids; Ketotifen; Leukotrienes; Lipoxygenase; Mice; ortho-Aminobenzoates; Peritoneal Cavity; Phospholipases A; Phospholipases A2; Phthalazines; Piperazines; Pyridazines; Thromboxanes | 1989 |
Mechanism of inhibitory action of tranilast on the release of slow reacting substance of anaphylaxis (SRS-A) in vitro: effect of tranilast on the release of arachidonic acid and its metabolites.
We investigated the mechanism of inhibitory action of tranilast, one of the anti-allergic drugs, on the release of slow reacting substance of anaphylaxis (SRS-A). Ionophore A23187 (0.5 or 0.2 micrograms/ml)-induced SRS-A release from rat peritoneal exudate cells (PEC) or human leucocytes was inhibited by tranilast (10(-5)-10(-3) M). The IC50 (the concentration which gives 50% inhibition) of tranilast on these reactions was approx. 10(-4) M. Prostaglandin (PG)E2 release from sensitized purified rat mast cells (PMC) by a specific antigen (DNP-Ascaris) was markedly suppressed by tranilast (10(-3) M). Similarly, ionophore A23187-induced PGE2 and 6-keto-PGF1 alpha releases from rat PEC were inhibited by tranilast (10(-5)-10(-3) M). DNP-Ascaris antigen-induced 3H-arachidonic acid (AA), 3H-PGE2, 3H-PGF2 alpha and 3H-PGD2 releases from rat PMC were markedly suppressed by tranilast (10(-5)-10(-3) M), DSCG (10(-5)-10(-4) M) and mepacrine (10(-3) M). The activity of AA-converting enzymes such as 5-lipoxygenase, cyclooxygenase, PGI2 synthetase, and glutathione-S-transferase was hardly influenced by tranilast (10(-5)-10(-3) M). From these results, we suggest that the mechanism of the inhibitory action of tranilast on the release of SRS-A is related to the processes prior to dissociation of AA from the membrane phospholipids. Topics: Animals; Arachidonate 5-Lipoxygenase; Arachidonic Acid; Arachidonic Acids; Aspirin; Calcimycin; Histamine; Humans; In Vitro Techniques; Leukocytes; Male; Mice; ortho-Aminobenzoates; Prostaglandin-Endoperoxide Synthases; Prostaglandins; Rats; Rats, Inbred Strains; SRS-A | 1988 |
Oxatomide inhibits the release of bronchoconstrictor arachidonic acid metabolites (iLTC4 and PGD2) from rat mast cells and guinea-pig lung.
The effect of oxatomide, an orally active antiallergic drug, on immunoreactive LTC4 (iLTC4) production has been studied in rat peritoneal exudate cells (PEC) and guinea-pig lung fragments using the calcium ionophore A23187 and specific antigen in vitro. Oxatomide (10(-5) M) inhibited iLTC4 release by 70% with A23187 from rat PEC, and by 48% with antigen from guinea-pig lung. Oxatomide is supposed to affect the biosynthesis pathway of leukotrienes, because oxatomide inhibits 5-lipoxygenase from guinea-pig peritoneal leukocytes with an IC50 17 microM. Oxatomide also depressed the release of PGD2 from rat peritoneal mast cells stimulated by A23187 (IC50 4.2 microM). The effects of oxatomide on iLTC4 and PGD2 release were more potent than other antiallergic drugs (DSCG, ketotifen, tranilast). Topics: Animals; Arachidonate 5-Lipoxygenase; Calcimycin; Cromolyn Sodium; Guinea Pigs; Ketotifen; Lung; Mast Cells; ortho-Aminobenzoates; Piperazines; Prostaglandin D2; Prostaglandin-Endoperoxide Synthases; Prostaglandins D; Rats; SRS-A | 1987 |
Effect of cinnarizine on IgE antibody mediated allergic reaction in mice and rats.
The effect of cinnarizine on immunoglobulin E (IgE) antibody mediated allergic reactions in mice and rats was investigated. Nifedipine and tranilast were used as comparative drugs. The dye leakage caused by IgE antibody mediated passive cutaneous anaphylaxis (PCA) in mouse ear was clearly inhibited by cinnarizine administered both orally and intraperitoneally. The inhibitory action of cinnarizine for PCA was as potent as nifedipine and superior to tranilast. Cinnarizine clearly inhibited the increase in capillary permeability caused by histamine and calcium ionophore A 23187 (A 23187) but not by LTD4 in mouse ear. Nifedipine inhibited the increases of capillary permeability caused by A 23187, histamine and LTD4. Tranilast inhibited A 23187 induced vasculitis but not histamine or LTD4-induced reaction. Cinnarizine had no significant effect on the release of histamine caused by antigen or A 23187 from rat peritoneal mast cells. Nifedipine and tranilast inhibited the release of histamine caused by both antigen and A 23187 from rat peritoneal mast cells. Topics: Animals; Calcimycin; Capillary Permeability; Cinnarizine; Female; Histamine Antagonists; Histamine Release; Immunoglobulin E; Male; Mast Cells; Mice; Mice, Inbred BALB C; Nifedipine; ortho-Aminobenzoates; Passive Cutaneous Anaphylaxis; Rats; Rats, Inbred Strains; SRS-A | 1986 |
Effect of N-5' on histamine release from rat peritoneal exudate cells induced by calcium ionophore and ATP.
We studied the effect of N-(3,4-dimethoxycinnamoyl)anthranilic acid (N-5'), an orally applicable anti-allergic drug, on the histamine release induced by calcium ionophores (A23187 and X537A) and ATP from rat peritoneal exudate cells (PEC). X537A (0.1-33.3 micrograms/ml) induced histamine release in a concentration-related manner, and 2.0 micrograms/ml of X537A induced release to the same extent as allergic histamine release. Histamine release induced by 2.0 micrograms/ml of X537A increased with longer incubation time, reaching a peak of about 100% at 120 min. N-5' had no effect on histamine release induced by X537A at the concentrations used (1-1000 microM), but DSCG exhibited significant inhibition at 1-100 microM. A23187 (0.05-0.5 microgram/ml) induced histamine release in a concentration-related manner, and it seemed that 0.033 microgram/ml of A23187 induces the same degree of histamine release as the allergic one. A23187 induced rapid histamine release which attained maximum 1 min after the addition. N-5' exhibited a significant concentration-dependent inhibitory effect on histamine release induced by A23187, and DSCG also exhibited significant inhibition (10 and 1000 microM). N-5' significantly inhibited histamine release induced by 100 microM ATP. These results indicate that N-5' and DSCG effect the histamine release induced by ionophore A23187 and X537A by different manners, and they suggest the possibility that N-5' inhibits some Ca++-dependent processes in histamine release, including the influx of Ca++ into cells, which is a trigger of the A23187 and ATP effects. Topics: Adenosine Triphosphate; Animals; Ascitic Fluid; Calcimycin; Dose-Response Relationship, Drug; Drug Interactions; Histamine; In Vitro Techniques; Ionophores; Lasalocid; ortho-Aminobenzoates; Rats | 1984 |
In vitro inhibition of histamine release from mouse mast cells and human basophils by an anthranilic acid derivative.
Optimal conditions for in vitro histamine release mediated either by Con A (3 micrograms/ml) or by Ionophore A23187 (1 microgram/ml), were established for mouse peritoneal mast cells and human normal basophils. In both systems N-5' exerts potent inhibiting effects on histamine release after short term (1-5 minutes) in vitro preincubation. At concentrations of 1mM for mouse mast cells and 3mM for normal human basophils, N-5' inhibits up to 95% Con A-induced histamine release and more than 50% ionophore-induced histamine release. Such in vitro effects are more potent than DSCG-mediated inhibition, under similar experimental conditions, and are resistant to challenge with exceeding doses of the two releasing agents, particularly in the Con A system. Interestingly, basophils with apparent normal morphology, from a CML patient, were resistant to both challenges. Topics: Animals; Basophils; Calcimycin; Cells, Cultured; Concanavalin A; Histamine Release; Humans; Mast Cells; Mice; ortho-Aminobenzoates | 1983 |