Suwa T, Nakazima M, Shinozaki A, Kyogoku K, Mori Y
Jpn J Pharmacol. 1984 May;35(1):47-53. doi: 10.1254/jjp.35.47.
The gastric cytoprotective action of SU-88, an anti-ulcer agent, was studied in rats. SU-88 dose-dependently prevented the formation of gastric lesions induced by absolute ethanol as observed by PGE2. The efficacy of SU-88 when given i.p. was more potent than the p.o. administration. Indomethacin (5mg/kg, p.o.) given 30 min prior to SU-88 dosing blocked this protective effect, whereas it was not affected when indomethacin was given 30 min after the SU-88 dosing. Cimetidine, on the other hand, failed to exert a protective effect against the ethanol-induced lesions and caused a significant increase in the lesions induced by 0.6N HCI. Pretreatment with SU-88 prior to cimetidine resulted in a marked reduction in the lesions. SU-88 was found to increase the synthesis of gastric glycoproteins and to prevent the reduction of glycoprotein synthesis caused by the administration of absolute ethanol. However, no increase in the synthesis was observed 5 min after the SU-88 dosing, although the lesion was significantly suppressed at that time. These findings indicate that SU-88 possesses a cytoprotective effect and that this effect seems to be mediated by the increase in endogenous PG.
对抗溃疡药物SU - 88在大鼠体内的胃细胞保护作用进行了研究。通过前列腺素E2（PGE2）观察发现，SU - 88呈剂量依赖性地预防了无水乙醇诱导的胃损伤形成。腹腔注射SU - 88的效果比口服给药更强。在SU - 88给药前30分钟口服吲哚美辛（5mg/kg）可阻断这种保护作用，而在SU - 88给药后30分钟给予吲哚美辛则不会影响其保护作用。另一方面，西咪替丁对乙醇诱导的损伤没有保护作用，反而会导致0.6N盐酸诱导的损伤显著增加。在西咪替丁给药前用SU - 88预处理可使损伤明显减轻。研究发现，SU - 88可增加胃糖蛋白的合成，并防止因给予无水乙醇而导致的糖蛋白合成减少。然而，在SU - 88给药后5分钟，虽然此时损伤已被显著抑制，但未观察到合成增加。这些发现表明，SU - 88具有细胞保护作用，且这种作用似乎是由内源性前列腺素的增加介导的。
