Goossens J, Van Reempts J, Van Wauwe J P
Br J Pharmacol. 1987 May;91(1):165-9. doi: 10.1111/j.1476-5381.1987.tb08995.x.
The cytoprotective effects of the anti-asthmatic drug, disodium cromoglycate (DSCG), on gastric mucosal necrosis induced by ethanol in rats were studied. Subcutaneous, but not oral, DSCG prevented the formation of gastric lesions and this effect was dose-dependent between 1.25 and 40 mg kg-1, with an ED50 value of 6.8 mg kg-1. Maximal cytoprotection occurred 15-30 min after DSCG treatment. Histological examination revealed that DSCG effectively protected the gastric mucosa against ethanol-induced vascular congestion, haemorrhage, epithelial desquamation and mucosal oedema. Enhanced production of endogenous prostaglandins, which are known cytoprotective compounds, could not explain the mucosal protection. At a dose of 40 mg kg-1, DSCG did not change prostaglandin E2 or 6-keto-prostaglandin F1 alpha concentrations in gastric mucosal tissue, although its cytoprotective activity was partially inhibited by prior treatment of the animals with indomethacin.
研究了抗哮喘药物色甘酸钠(DSCG)对乙醇诱导的大鼠胃黏膜坏死的细胞保护作用。皮下注射而非口服DSCG可预防胃损伤的形成,且该作用在1.25至40 mg kg-1之间呈剂量依赖性,ED50值为6.8 mg kg-1。DSCG治疗后15 - 30分钟出现最大细胞保护作用。组织学检查显示,DSCG有效地保护胃黏膜免受乙醇诱导的血管充血、出血、上皮脱落和黏膜水肿。内源性前列腺素生成增加,而前列腺素是已知的细胞保护化合物,但这并不能解释黏膜保护作用。在40 mg kg-1的剂量下,DSCG并未改变胃黏膜组织中前列腺素E2或6-酮-前列腺素F1α的浓度,尽管用吲哚美辛预先处理动物可部分抑制其细胞保护活性。