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硫糖铝对胃黏膜乙醇诱导损伤的保护作用:是前列腺素介导的过程吗?

Sucralfate protection of the gastric mucosa against ethanol-induced injury: a prostaglandin-mediated process?

作者信息

Hollander D, Tarnawski A, Gergely H, Zipser R D

出版信息

Scand J Gastroenterol Suppl. 1984;101:97-102.

PMID:6599542
Abstract

We studied whether sucralfate's protection of the gastric mucosa against ethanol induced injury in the rat is prostaglandin mediated. Rats received intragastric pretreatment: i) saline, ii) sucralfate, and iii) indomethacin-sucralfate. One hour later gastric contents were obtained for measurements of prostaglandin E2 and 2 ml of 100% ethanol were instilled. Rats were sacrificed 1 h later. The gastric mucosa was assessed: a) macroscopically by planimetry, b) by quantitative histology, and c) by measurements of gastric volume, pH and sodium. We found that sucralfate significantly increased gastric luminal release of prostaglandin E2. The increase was completely abolished by indomethacin pretreatment. Sucralfate protected the gastric mucosa against ethanol injury reducing macroscopic and histologic necrosis. Indomethacin (prostaglandin synthetase inhibitor) given 2 h prior to sucralfate markedly abolished its protective action against ethanol induced necrosis by 70%. These findings indicate that prostaglandins mediate some of the protective action of sucralfate. Sucralfate appears to have additional protective action which is prostaglandin independent.

摘要

我们研究了硫糖铝对大鼠胃黏膜乙醇诱导损伤的保护作用是否由前列腺素介导。大鼠接受胃内预处理:i)生理盐水,ii)硫糖铝,iii)吲哚美辛-硫糖铝。1小时后获取胃内容物用于测量前列腺素E2,并注入2ml 100%乙醇。1小时后处死大鼠。对胃黏膜进行评估:a)通过面积测量法进行宏观评估,b)通过定量组织学评估,c)通过测量胃容量、pH值和钠含量。我们发现硫糖铝显著增加胃腔内前列腺素E2的释放。吲哚美辛预处理可完全消除这种增加。硫糖铝保护胃黏膜免受乙醇损伤,减少宏观和组织学坏死。在硫糖铝给药前2小时给予吲哚美辛(前列腺素合成酶抑制剂),可使硫糖铝对乙醇诱导坏死的保护作用显著降低70%。这些发现表明前列腺素介导了硫糖铝的部分保护作用。硫糖铝似乎还有与前列腺素无关的额外保护作用。

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