Schmidt K L, Henagan J M, Smith G S, Hilburn P J, Miller T A
Gastroenterology. 1985 Mar;88(3):649-59. doi: 10.1016/0016-5085(85)90132-5.
Using macroscopic criteria for injury, prostaglandins have been alleged to possess potent antiulcer properties despite meager histologic evidence for this cytoprotective action. This time-sequence study used light, scanning, and transmission electron microscopy to evaluate the effects of 16,16-dimethyl prostaglandin E2 on gastric mucosal integrity after exposure to 100% ethanol. Macroscopically, virtually complete protection against injury to the glandular mucosa of the in vivo rat stomach was noted in animals receiving 10 micrograms/kg body wt of prostaglandin subcutaneously before oral ethanol administration when killed at 5, 20, and 60 min after ethanol exposure compared with oral ethanol after saline injection. On light microscopy the length of injured epithelium in prostaglandin/ethanol- and saline/ethanol-treated tissues was not significantly different at all time periods studied. Although the depth of injury extended into gastric glands in both groups killed at 5 min, the deep pit surface mucus cells in prostaglandin/ethanol mucosa were less damaged and necrotic lesions were virtually absent when compared with saline/ethanol mucosa. At 20 and 60 min, cellular injury could still be identified in prostaglandin/ethanol-treated mucosa but the depth of injury became even less pronounced over time in contrast to mucosa exposed to ethanol without prostaglandin. Scanning electron microscopy and transmission electron microscopy confirmed these differences. Despite the macroscopic findings, these results indicate that prostaglandin does not prevent superficial surface mucus cell necrosis in ethanol-exposed mucosa even though it does spare cells in the pit base. The reduction in damaged cells over time in prostaglandin/ethanol-treated mucosa, in contrast to saline/ethanol-treated mucosa, supports the hypothesis that the reepithelialization of the lamina propria is initiated by spared deep-lying pit cells.
依据损伤的宏观标准,尽管关于这种细胞保护作用的组织学证据不足,但前列腺素据称具有强大的抗溃疡特性。这项时间序列研究运用光学显微镜、扫描电子显微镜和透射电子显微镜,来评估16,16 - 二甲基前列腺素E2对100%乙醇暴露后胃黏膜完整性的影响。宏观上,在口服乙醇前皮下注射10微克/千克体重前列腺素的动物中,与注射生理盐水后口服乙醇的动物相比,在乙醇暴露后5分钟、20分钟和60分钟处死时,发现其对体内大鼠胃腺黏膜损伤具有几乎完全的保护作用。光学显微镜观察显示,在所有研究时间段,前列腺素/乙醇处理组和生理盐水/乙醇处理组组织中受损上皮的长度并无显著差异。尽管在5分钟处死的两组中,损伤深度均延伸至胃腺,但与生理盐水/乙醇处理的黏膜相比,前列腺素/乙醇处理的黏膜中深窝表面黏液细胞受损较轻,几乎没有坏死病变。在20分钟和60分钟时,仍可在前列腺素/乙醇处理的黏膜中识别出细胞损伤,但与未用前列腺素处理的乙醇暴露黏膜相比,随着时间推移,损伤深度变得更不明显。扫描电子显微镜和透射电子显微镜证实了这些差异。尽管有宏观观察结果,但这些结果表明,前列腺素并不能防止乙醇暴露黏膜中表面黏液细胞的坏死,即便它确实能使窝底部的细胞免受损伤。与生理盐水/乙醇处理的黏膜相比,前列腺素/乙醇处理的黏膜中受损细胞随时间减少,这支持了固有层再上皮化由保留的深层窝细胞启动的假说。