Mizui T, Doteuchi M
Jpn J Pharmacol. 1983 Oct;33(5):939-45. doi: 10.1254/jjp.33.939.
The participation of polyamines and nonprotein sulfhydryls in the gastric cytoprotective mechanisms was studied using gastric mucosal lesions produced by acidified ethanol in rats as an experimental model. Treatment with prostaglandin E2 (PGE2), but not cimetidine, prevented the formation of gastric mucosal lesions. Oral administration of cadaverine, spermidine and spermine prevented the lesion formation by acidified ethanol in a dose-dependent manner. Indomethacin or acetazolamide had no influence on the cytoprotective effect of spermine, whereas sulfhydryl blockers such as iodoacetamide and N-ethylmaleimide partially blocked it. Sulfhydryl compounds such as cysteine, reduced glutathione (GSH), and cysteamine prevented the lesion formation induced by acidified ethanol. The concentration of nonprotein sulfhydryls in the gastric mucosa was significantly decreased at 1 hr after administration of acidified ethanol, and this decrease was partially prevented by spermine or PGE2. These results suggest that the cytoprotective effect of spermine may not be mediated by endogenous prostaglandins or alkaline secretion in the gastric mucosa, but may be partially related to endogenous sulfhydryl compounds.
以大鼠酸化乙醇所致胃黏膜损伤作为实验模型，研究了多胺和非蛋白巯基在胃细胞保护机制中的作用。前列腺素E2（PGE2）治疗可预防胃黏膜损伤形成，而西咪替丁则无此作用。口服尸胺、亚精胺和精胺可剂量依赖性地预防酸化乙醇所致的损伤形成。吲哚美辛或乙酰唑胺对精胺的细胞保护作用无影响，而碘乙酰胺和N-乙基马来酰亚胺等巯基阻断剂可部分阻断该作用。半胱氨酸、还原型谷胱甘肽（GSH）和半胱胺等巯基化合物可预防酸化乙醇所致的损伤形成。给予酸化乙醇1小时后，胃黏膜中非蛋白巯基的浓度显著降低，而精胺或PGE2可部分预防这种降低。这些结果表明，精胺的细胞保护作用可能不是由内源性前列腺素或胃黏膜碱性分泌介导的，而是可能部分与内源性巯基化合物有关。
