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关于半胱胺诱导大鼠十二指肠溃疡形成的生化背景

On the biochemical background of cysteamine-induced duodenal ulceration in the rat.

作者信息

Balint G A

机构信息

Dept. of Neurology and Psychiatry, Albert Szent-Györgyi Medical University, Szeged, Hungary.

出版信息

Scand J Gastroenterol. 1993 May;28(5):423-6. doi: 10.3109/00365529309098243.

DOI:10.3109/00365529309098243
PMID:7685539
Abstract

In cysteamine-induced duodenal ulceration the endogenous prostacyclin level initially showed an elevation. This elevation later disappeared, and the endogenous prostacyclin level dropped to zero--that is, below the detection limit. During ulceration the mucosal DNA level decreased, a phenomenon that was directly proportional to ulceration. In the course of the ulcerative process in the duodenal mucosa a de novo protein synthesis took place. This process was most probably a mucus secretion and served as a protective reaction against damaging noxae. The mucosal cyclic adenosine 5'-monophosphate (cAMP) content increased in the so-called pre-ulcerative phase but later returned to the normal (physiologic) level. The changes in the cyclic guanosine 5'-monophosphate (cGMP) level were more pronounced than those of cAMP, and the final result was a decrease in the mucosal cAMP/cGMP ratio. In accordance with our previous results we conclude that a positive cAMP/cGMP 'shift' indicates antiulcerogenic, cytoprotective, reparative processes in the mucosa, whereas its decrease is connected to damaging noxae.

摘要

在半胱胺诱导的十二指肠溃疡形成过程中,内源性前列环素水平最初呈现升高。这种升高随后消失,内源性前列环素水平降至零,即低于检测限。溃疡形成期间,黏膜DNA水平下降,这一现象与溃疡形成直接相关。在十二指肠黏膜溃疡过程中发生了从头蛋白质合成。这个过程很可能是黏液分泌,起到了针对有害刺激的保护反应作用。黏膜环磷酸腺苷(cAMP)含量在所谓的溃疡前期增加,但随后恢复到正常(生理)水平。环磷酸鸟苷(cGMP)水平的变化比cAMP更明显,最终结果是黏膜cAMP/cGMP比值降低。根据我们之前的结果,我们得出结论,cAMP/cGMP的正向“转变”表明黏膜中存在抗溃疡、细胞保护和修复过程,而其降低与有害刺激相关。

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