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16,16-二甲基前列腺素E2对大鼠乙醇诱导和阿司匹林诱导的胃损伤的影响。扫描电子显微镜研究。

Effects of 16,16-dimethyl prostaglandin E2 on ethanol-induced and aspirin-induced gastric damage in the rat. Scanning electron microscopic study.

作者信息

Ohno T, Ohtsuki H, Okabe S

出版信息

Gastroenterology. 1985 Jan;88(1 Pt 2):353-61. doi: 10.1016/s0016-5085(85)80189-x.

Abstract

Ethanol and aspirin were administered orally to fasted rats and the effects of 16,16-dimethyl prostaglandin E2 (given orally as a pretreatment) were studied using scanning electron microscopy. Gastric secretory studies (pylorus ligation for 2 h) showed that 3 and 30 micrograms/kg of 16,16-dimethyl prostaglandin E2 were nonantisecretory doses and that 100 micrograms/kg was an antisecretory dose. 16,16-Dimethyl prostaglandin E2, given orally at 3-100 micrograms/Kg, induced no appreciable changes in the gastric surface epithelial cells. Oral administration of 1 ml of 50% ethanol invariably induced, within 10 min, extensive exfoliation of surface epithelial cells throughout the corpus and antrum and exposed the lamina propria. 16,16-Dimethyl prostaglandin E2, given orally at 3, 30, and 100 micrograms/kg 30 min before ethanol treatment, had no protective effect. Aspirin, given orally at 30 or 100 mg/kg, also damaged the surface epithelium of both the corpus and the antrum within 10 min. This damage ranged from apical cellular erosions to widespread exposure of the lamina propria. 16,16-Dimethyl prostaglandin E2, given orally at 3 or 30 micrograms/kg 30 min before aspirin treatment, significantly inhibited the gastric damage induced by both 30 and 100 mg/kg of aspirin. The inhibition of damage index was about 50%-60% at either 30 or 100 micrograms/kg of 16,16-dimethyl prostaglandin E2. The mechanism of the protection seen with 16,16-dimethyl prostaglandin E2 remains to be determined.

摘要

将乙醇和阿司匹林经口给予禁食的大鼠,并使用扫描电子显微镜研究16,16 - 二甲基前列腺素E2(经口给予作为预处理)的作用。胃分泌研究(幽门结扎2小时)表明,3微克/千克和30微克/千克的16,16 - 二甲基前列腺素E2为非抗分泌剂量,而100微克/千克为抗分泌剂量。以3 - 100微克/千克经口给予16,16 - 二甲基前列腺素E2,未引起胃表面上皮细胞出现明显变化。经口给予1毫升50%乙醇,在10分钟内总会导致整个胃体和胃窦的表面上皮细胞广泛脱落,使固有层暴露。在乙醇处理前30分钟经口给予3微克/千克、30微克/千克和100微克/千克的16,16 - 二甲基前列腺素E2,没有保护作用。以30毫克/千克或100毫克/千克经口给予阿司匹林,在10分钟内也会损伤胃体和胃窦的表面上皮。这种损伤范围从顶端细胞糜烂到固有层广泛暴露。在阿司匹林处理前30分钟经口给予3微克/千克或30微克/千克的16,16 - 二甲基前列腺素E2,可显著抑制由30毫克/千克和100毫克/千克阿司匹林引起的胃损伤。在30微克/千克或100微克/千克的16,16 - 二甲基前列腺素E2时,损伤指数的抑制率约为50% - 60%。16,16 - 二甲基前列腺素E2产生保护作用的机制尚待确定。

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