Jentjens T, Smits H L, Strous G J
Gastroenterology. 1984 Aug;87(2):409-16.
It has been suggested that the cytoprotective effect of prostaglandins could be mediated by an increased mucus glycoprotein secretion in the stomach. In the rat we studied the mucus glycoprotein synthesis after an in vivo treatment with 16,16-dimethyl prostaglandin E2 (10 micrograms/kg X day subcutaneously) for 1 h or 7 days. The incorporation rate of [3H]galactose, [3H]glucosamine, and [3H]serine was determined by light microscopic autoradiography in the ex vivo vascularly perfused stomach. Prostaglandin increased the rate of [3H]galactose and [3H]glucosamine incorporation twofold to fourfold in the fundic surface mucous cells; but the total protein synthesis as measured by [3H]serine incorporation was not increased. Analyses of purified mucus glycoprotein did not show an effect on carbohydrate composition, oligosaccharide chain size, nor on buoyant density, after prostaglandin treatment. The present study reveals that 16,16-dimethyl prostaglandin E2 stimulates the mucus glycoprotein synthesis in the fundic mucous cells. This effect may well be one of the mechanisms by which prostaglandin protects the stomach against noxious agents.
有人提出,前列腺素的细胞保护作用可能是通过增加胃黏液糖蛋白的分泌来介导的。在大鼠体内,我们研究了用16,16-二甲基前列腺素E2(10微克/千克×天,皮下注射)进行1小时或7天的体内治疗后黏液糖蛋白的合成情况。通过光学显微镜放射自显影法测定离体血管灌注胃中[3H]半乳糖、[3H]葡糖胺和[3H]丝氨酸的掺入率。前列腺素使胃底表面黏液细胞中[3H]半乳糖和[3H]葡糖胺的掺入率增加了两倍至四倍;但通过[3H]丝氨酸掺入测定的总蛋白质合成并未增加。对纯化的黏液糖蛋白进行分析发现,前列腺素处理后,其碳水化合物组成、寡糖链大小或浮力密度均未受到影响。本研究表明,16,16-二甲基前列腺素E2可刺激胃底黏液细胞中黏液糖蛋白的合成。这种作用很可能是前列腺素保护胃免受有害因子侵害的机制之一。