首页> 外文期刊>Japanese Journal of Pharmacology >Prostaglandin D2 Generation by Rat Peritoneal Mast Cells Stimulated With Datura stramonium Agglutinin and Its Inhibition by Haptenic Sugar and Wheat Germ Agglutinin
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Prostaglandin D2 Generation by Rat Peritoneal Mast Cells Stimulated With Datura stramonium Agglutinin and Its Inhibition by Haptenic Sugar and Wheat Germ Agglutinin

机译:曼陀罗凝集素刺激大鼠腹膜肥大细胞产生前列腺素D2及其对半乳糖和小麦胚芽凝集素的抑制作用

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References(11) Cited-By(1) The production of prostaglandin D2 (PGD2) by rat peritoneal mast cells incubated with N-acetyl glucosamine (GlcNAc) oligomer-specific Datura stramonium agglutinin (DSA) for 10 min in the presence of 0.3 mM Ca2+ was examined. Previously, our group reported that the incubation of rat mast cells with DSA (5 – 100 μg/ml) under similar conditions resulted in a calcium influx and histamine release via a pertussis toxin-sensitive G-protein pathway of the mast cells, and the histamine release was inhibited by haptenic sugar chitooligosaccharides or GlcNAc-specific lectin wheat germ agglutinin (WGA) (K. Matsuda et al., Jpn J Pharmacol 66, 195 – 204 (1994)). DSA (5 – 100 μg/ml) dose-dependently stimulated the mast cells to generate PGD2. Chitooligosaccharides (1% w/v) and WGA (100 μg/ml) inhibited the production of PGD2 induced by 100 μg/ml of DSA, suggesting that the effect of DSA is sugar-specific. A prostaglandin G/H synthase inhibitor NS-398 (N-[cyclohexyloxy-4-nitrophenyl] methanesulfonamide) (10 μM) inhibited the formation of PGD2 induced by DSA (20 μg/ml). These results suggest that the binding of DSA to the corresponding sugar residues on the mast cell surface mediates the signaling of the prostaglandin G/H synthase pathway.
机译:参考文献(11)(1)在0.3 mM存在下,大鼠腹膜肥大细胞与N-乙酰氨基葡糖(GlcNAc)低聚物特异性曼陀罗草铵凝集素(DSA)孵育10分钟产生前列腺素D2(PGD2)。检查了Ca2 +。先前,我们的小组报告说,在相似条件下用DSA(5 – 100μg/ ml)孵育大鼠肥大细胞会导致钙肥大和组胺通过肥大细胞的百日咳毒素敏感性G蛋白途径释放出来,并且组胺的释放被半抗原糖壳寡糖或GlcNAc特异性凝集素小麦胚芽凝集素(WGA)抑制(K. Matsuda等人,Jpn J Pharmacol 66,195 – 204(1994))。 DSA(5 – 100μg/ ml)剂量依赖性地刺激肥大细胞产生PGD2。壳寡糖(1%w / v)和WGA(100μg/ ml)抑制了100μg/ ml DSA诱导的PGD2的产生,表明DSA的作用是糖特异性的。前列腺素G / H合酶抑制剂NS-398(N- [环己氧基-4-硝基苯基]甲磺酰胺)(10μM)抑制了DSA诱导的PGD2的形成(20μg/ ml)。这些结果表明,DSA与肥大细胞表面上相应的糖残基的结合介导了前列腺素G / H合酶途径的信号传导。

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