胃黏膜巯基在柳氮磺胺吡啶溃疡保护作用中的角色。
The role of the gastric mucosal sulfhydryls in the ulcer-protecting effects of sulphasalazine.
作者信息
Garg G P, Cho C H, Ogle C W
机构信息
Department of Pharmacology, Faculty of Medicine, University of Hong Kong.
出版信息
J Pharm Pharmacol. 1991 Oct;43(10):733-4. doi: 10.1111/j.2042-7158.1991.tb03469.x.
The role of gastric mucosal sulfhydryls in gastric ulceration, produced by restraint at 4 degrees C (stress) for 2 h, and in the ulcer-protecting effects of sulphasalazine and its constituents (sulphapyridine and 5-aminosalicylic acid), have been studied in rats. Stress significantly raised the mucosal sulphydryl content, but sulphasalazine and sulphapyridine did not influence these changes; only 5-aminosalicylic acid decreased the mucosal sulphydryl concentration. These results indicate that depletion of mucosal sulfhydryls does not occur in stress-induced ulceration, in contrast to what has been shown in other experimental ulcer models. The antiulcer effects of sulphasalazine or of any of its constituents may, therefore, not involve the sulphydryl mechanism.
研究了胃黏膜巯基在4℃束缚应激2小时所致大鼠胃溃疡形成中的作用，以及柳氮磺胺吡啶及其成分（磺胺吡啶和5-氨基水杨酸）的溃疡保护作用。应激显著提高了黏膜巯基含量，但柳氮磺胺吡啶和磺胺吡啶并未影响这些变化；只有5-氨基水杨酸降低了黏膜巯基浓度。这些结果表明，与其他实验性溃疡模型不同，应激诱导的溃疡形成过程中并未出现黏膜巯基的耗竭。因此，柳氮磺胺吡啶或其任何成分的抗溃疡作用可能不涉及巯基机制。
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