Cook G A, Elliott S L, Skeljo M V, Giraud A S, Yeomans N D
University of Melbourne, Department of Medicine, Australia.
Dig Dis Sci. 1997 Mar;42(3):654-60. doi: 10.1023/a:1018828016573.
Prostaglandins protect the gastric mucosa against a variety of injurious agents and may accelerate the recovery of the gastric mucosa following damage. In previous studies prostaglandins were given prior to the injurious agent, so it was not possible to distinguish their potential effects on accelerating repair or reducing initial damage. We have investigated the effect of 16,16-dimethyl prostaglandin E2 (dmPGE2) on the repair of the gastric mucosa after injury induced by several injurious agents. dmPGE2 was given orally 15 min prior to aspirin or sodium salicylate, or 30 min after aspirin, sodium salicylate, or ethanol. dmPGE2 delivered prior to injury reduced the aspirin-induced fall in mucosal potential difference (PD), but had no effect on that induced by sodium salicylate. dmPGE2 administered after ASA injury significantly increased recovery of PD (P < 0.05), but did not alter the rate of recovery of PD with other damaging agents. Histological damage was decreased in rats treated with dmPGE2 after aspirin compared to aspirin-only-treated rats (P < 0.02). Exogenous dmPGE2 protects and restores gastric mucosal integrity after aspirin damage but has no effect on the repair of sodium salicylate and ethanol injured mucosa, suggesting that repair of the gastric mucosa after aspirin damage is enhanced by dmPGE2 due to its ability to prevent ongoing damage, rather than directly enhancing repair processes.
前列腺素可保护胃黏膜免受多种损伤因子的侵害,并可能加速胃黏膜损伤后的恢复。在以往的研究中,前列腺素是在损伤因子之前给予的,因此无法区分它们在加速修复或减少初始损伤方面的潜在作用。我们研究了16,16 - 二甲基前列腺素E2(dmPGE2)对几种损伤因子诱导的胃黏膜损伤修复的影响。在给予阿司匹林或水杨酸钠前15分钟口服dmPGE2,或在给予阿司匹林、水杨酸钠或乙醇后30分钟口服dmPGE2。损伤前给予dmPGE2可减轻阿司匹林诱导的黏膜电位差(PD)下降,但对水杨酸钠诱导的电位差下降没有影响。阿司匹林损伤后给予dmPGE2可显著提高PD的恢复率(P < 0.05),但不改变其他损伤因子导致的PD恢复速率。与仅用阿司匹林治疗的大鼠相比,阿司匹林损伤后用dmPGE2治疗的大鼠组织学损伤减轻(P < 0.02)。外源性dmPGE2可保护并恢复阿司匹林损伤后的胃黏膜完整性,但对水杨酸钠和乙醇损伤的黏膜修复没有影响,这表明dmPGE2可增强阿司匹林损伤后胃黏膜的修复,是因为其具有防止持续损伤的能力,而非直接增强修复过程。