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幽门螺杆菌脂多糖导致清醒大鼠胃排空延迟。

Delayed gastric emptying by Helicobacter pylori lipopolysaccharide in conscious rats.

作者信息

Okumura T, Shoji E, Takahashi N, Wakebe H, Imagawa K, Kikuchi M, Kohgo Y

机构信息

Third Department of Internal Medicine, Asahikawa Medical College, Hokkaido, Japan.

出版信息

Dig Dis Sci. 1998 Jan;43(1):90-4. doi: 10.1023/a:1018828105226.

Abstract

The present study was carried out to investigate the possibility that lipopolysaccharide deprived from Helicobacter pylori may alter gastric motility. To address the question, we examined the effect of H. pylori lipopolysaccharide on gastric emptying in conscious rats. Gastric emptying was evaluated by the phenol red method. Time-course and dose-related effects of intraperitoneal administration of H. pylori lipopolysaccharide were investigated. Intraperitoneal injection of H. pylori lipopolysaccharide significantly suppressed gastric emptying of a liquid meal in a dose-dependent manner. The inhibitory action of H. pylori lipopolysaccharide was observed 2, 4, 8, or 12 hr after the injection. These results suggest for the first time that H. pylori lipopolysaccharide may suppress gastric emptying in a long-lasting fashion. It is also suggested that H. pylori may influence gastric function through its cell wall structure named lipopolysaccharide.

摘要

本研究旨在探讨幽门螺杆菌来源的脂多糖是否可能改变胃动力。为解决该问题,我们检测了幽门螺杆菌脂多糖对清醒大鼠胃排空的影响。采用酚红法评估胃排空情况。研究了腹腔注射幽门螺杆菌脂多糖的时间进程和剂量相关效应。腹腔注射幽门螺杆菌脂多糖以剂量依赖方式显著抑制流食的胃排空。注射后2、4、8或12小时观察到幽门螺杆菌脂多糖的抑制作用。这些结果首次表明,幽门螺杆菌脂多糖可能长期抑制胃排空。还表明幽门螺杆菌可能通过其名为脂多糖的细胞壁结构影响胃功能。

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