巯基物质在消炎痛诱发大鼠胃粘膜损伤中的作用

THE ROLE OF SULFHYDRYLS IN INDOMETHACIN-INDUCED GASTRIC MUCOSAL INJURY IN RATS

本工作研究了巯基物质在消炎痛引起大鼠胃粘膜损伤中的可能作用。在胃粘膜损伤发生过程中、胃粘膜内非蛋白及蛋白结合的巯基物质含量均无明显降低。虽然半胱胺灌胃(132或264μmol)或皮下注射(132μmol)后均明显抑制消炎痛溃疡的发生,其抑制率分别为82％,92％和75％,但同样具有巯基的半胱氨酸却无保护作用。半胱胺(132μmol)皮下注射可使消炎痛大鼠胃酸分泌抑制46％,而灌胃则无此作用。两种途径给予的半胱胺均不影响胃壁结合粘液的分泌。这些结果表明,胃粘膜内巯基物质似不参与消炎痛的致溃疡过程。半胱胺在此种模型上虽有强烈的细胞保护作用,但似乎不是由于其分子上所带的巯基所致。因此,巯基物质在消炎痛引起的胃粘膜损伤模型上没有细胞保护作用。

The possible role of sulfhydryls in indomethacin-induced gastric mucosal injury was studied. No significant decrease of the contents of both non-protein and protein-binding sulfhydryls was observed in the gastric mucosa during injury. Indomethacin-induced gastric ulcer was inhibited by cysteamine of 132 and 264μmol, i.g.or of 132μmol,s.c. by82％, 92％ and 75％ respectively. Such protective effect was not observed with cysteine in equal molar dose. Subcutaneously injected cysteamine (132 μmol) inhibited gastric acid secretion by 46％ in indomethacin-treated rats,while no effect was observed on acid secretion when cysteamine was given intragastrically. Cysteamine, given through both routes, did not affect gastric barrier mucus secretion. It is suggested that sulfhydryls in gastric mucosa are not involved in the mechanism of indomethacin-induced injury and that the potent cytoprotective effect of cysteamine against indomethacin-induced ulcer maybe not caused by its sulfhydral group.