幽门螺杆菌脂多糖对胃粘膜层粘连蛋白受体的抑制作用:尼替卡酮的作用。

B L Slomiany, J Piotrowski, G Rajiah, A Slomiany
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引用次数: 22

摘要

1. 利用sepharose结合的层粘连蛋白亲和层粘连蛋白层粘连蛋白从上皮细胞膜中分离出一个胃粘膜层粘连蛋白受体,放射性碘化后将其掺入脂质体中,对层粘连蛋白包被表面表现出特定的亲和性。2. 幽门螺杆菌脂多糖抑制脂质体受体与层粘连蛋白包被表面的结合,在50微克/毫升时达到96%的最大值。3.抗溃疡剂尼替卡酮可阻止幽门螺杆菌脂多糖对受体-层粘连蛋白结合的抑制作用。该效应具有浓度依赖性,在药物浓度为30微克/毫升时产生的最大应答率为83%。4. 结果表明,幽门螺杆菌能够通过干扰上皮细胞-层粘连蛋白结合来破坏胃粘膜的完整性,而抗核剂尼替卡酮可以抵消这种影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Inhibition of gastric mucosal laminin receptor by Helicobacter pylori lipopolysaccharide: effect of nitecapone.

1. A gastric mucosal laminin receptor has been isolated from the epithelial cell membrane by affinity chromatography on Sepharose-bound laminin, and following radioiodination was incorporated into liposomes which displayed specific affinity towards the laminin-coated surface. 2. The binding of liposomal receptor to the laminin-coated surface was inhibited by Helicobacter pylori lipopolysaccharide and reached a maximum value of 96% at 50 micrograms/ml. 3. The inhibitory effect of H. pylori lipopolysaccharide on the receptor-laminin binding was prevented by an antiulcer agent, nitecapone. The effect was concentration dependent and produced a maximum response of 83% at 30 micrograms/ml of drug concentration. 4. The results demonstrate that H. pylori is capable of disrupting gastric mucosal integrity by interfering with epithelial cell-laminin binding, and that an antiucler agent, nitecapone, counteracts this effect.

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