High Rate of IgE-Mediated Histamine Release from Rat Mesenteric Mast Cells.

Abstract

IgE-dependent histamine release from rat mesenteric mast cells was investigated. Excised mesenterium was cut into pieces and incubated with IgE overnight at 4°C for sensitization. Over 10 pieces of mesenterium specimen could be prepared from a rat. Antigen-induced histamine release from mesenterium specimen was initiated rapidly and reached a plateau in 5 min. In an optimal condition, over 50% of total histamine was released. In contrast, unpurified and purified peritoneal mast cells released only 22.5% and 5.3% of total histamine, respectively, upon IgE stimulation. Tranilast, a mast cell stabilizer, inhibited the histamine release from mesenteric mast cells significantly. The mesenterium might be a useful material for studying tissue-associated mast cell activation.

Tranilast Inhibits Glucose-induced Insulin Secretion from Pancreatic β-Cells

“…Because increased glucose uptake is suggested to accumulate glycolytic fl ux, leading to increasing ATP production, the suppression of mitochondrial metabolism by tranilast might cause a decrease in the ATP content in INS-1E cells. The concentration of tranilast we used is comparable with the concentration (100 mol / l -1 mmol / l) in which tranilast exerts an inhibitory effect on the release of chemical mediators, including histamine and prostaglandin E 2 , from mast cells [7,8] and is a therapeutically relevant concentration [20] . In summary, we demonstrated that tranilast, which is used as a drug for allergy, inhibited glucose-or tolbutamide-induced insulin secretion through the activation of K ATP channels in pancreatic -cells.…”