Fujimoto N, Murakami S, Suwa T, Mori Y
J Pharmacobiodyn. 1984 Nov;7(11):864-71. doi: 10.1248/bpb1978.7.864.
The gastric cytoprotective action of prostaglandin E2 (PGE2) and sofalcone was studied in rats. The in vitro incorporating activity of 3H-glucosamine into the gastric macromolecular glycoproteins was examined when PGE2 (0.1 mg/kg, p.o.) or sofalcone (100 mg/kg, i.p.) was administered 5, 15 or 30 min before the oral administration of absolute ethanol. The cytoprotective effect of PGE2 against gastric mucosal damage was demonstrated 5 min after PGE2 was given orally. The cytoprotective effect by sofalcone was seen after 15 min. However, during this period, the decrease in gastric macromolecular glycoprotein synthesis induced by the ethanol damage could not be restored by pretreatment with PGE2 or sofalcone. On the other hand, the reduction in the content of the gastric macromolecular glycoproteins by the ethanol damage was found to be prevented to a significant extent by pretreatment with PGE2. The same phenomenon was also observed in the administration of sofalcone. Accordingly, PGE2 has stimulating effect on the gastric glycoproteins biosynthesis, but this effect can not be considered as the mechanism responsible for cytoprotection, if indeed a single mechanism exists. Thus, it is suggested that the adhesion or maintenance of secreted macromolecular glycoproteins to the gastric tissue is closely related to cytoprotection.
在大鼠中研究了前列腺素E2（PGE2）和索法酮的胃细胞保护作用。在口服无水乙醇前5、15或30分钟给予PGE2（0.1mg/kg，口服）或索法酮（100mg/kg，腹腔注射），然后检测3H-葡萄糖胺掺入胃大分子糖蛋白的体外掺入活性。口服PGE2 5分钟后显示出PGE2对胃黏膜损伤的细胞保护作用。索法酮的细胞保护作用在15分钟后出现。然而，在此期间，乙醇损伤诱导的胃大分子糖蛋白合成减少不能通过PGE2或索法酮预处理恢复。另一方面，发现乙醇损伤引起的胃大分子糖蛋白含量降低在很大程度上可被PGE2预处理阻止。索法酮给药时也观察到相同现象。因此，PGE2对胃糖蛋白生物合成有刺激作用，但如果确实存在单一机制，这种作用不能被视为细胞保护的机制。因此，提示分泌的大分子糖蛋白与胃组织的黏附或维持与细胞保护密切相关。
