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:Datura stramonium凝集素刺激大鼠腹膜肥大细胞产生前列腺素D2,并受到半抗原和小麦胚芽凝集素的抑制。

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摘要

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 microg/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 microg/ml) dose-dependently stimulated the mast cells to generate PGD2. Chitooligosaccharides (1% w/v) and WGA (100 microg/ml) inhibited the production of PGD2 induced by 100 microg/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 microM) inhibited the formation of PGD2 induced by DSA (20 microg/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:在0.3 mM Ca2 +存在下,将与N-乙酰氨基葡萄糖(GlcNAc)低聚物特异性曼陀罗粘质凝集素(DSA)孵育10分钟的大鼠腹膜肥大细胞检测前列腺素D2(PGD2)的产生。先前,我们的小组报告说,在相似的条件下用DSA(5-100 microg / ml)孵育大鼠肥大细胞会通过肥大细胞的百日咳毒素敏感性G蛋白途径导致钙内流和组胺释放,并且组胺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(5-100 microg / ml)剂量依赖性地刺激肥大细胞产生PGD2。壳寡糖(1%w / v)和WGA(100微克/毫升)抑制了100微克/毫升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)(10 microM)抑制DSA诱导的PGD2的形成(20 microg / 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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