Domschke S, Dembiński A, Domschke W
Scand J Gastroenterol. 1983 Jan;18(1):113-6. doi: 10.3109/00365528309181569.
Biopsies were taken endoscopically from the fundic, antral, and upper duodenal region of healthy volunteers and gastric ulcer patients and were incubated in carbogen-saturated and buffered Medium 199 at 37 degrees C. The rate of DNA synthesis, estimated as incorporation of tritiated thymidine into tissue DNA, was determined as an index of cellular integrity. During the 30-min incubation, ethanol (25% v/v) significantly (p less than 0.01) depressed DNA synthesis by about 50% in the gastroduodenal mucosa of normal subjects and even by two thirds in the gastric mucosa of gastric ulcer patients. Prostaglandin E2 (PGE2) by itself (1 mg/50 ml) had no stimulatory effect on DNA synthesis; it did, however, reduce the drastic fall in DNA synthesis due to ethanol (p less than 0.005) when administered concomitantly. The basic process underlying cytoprotection by PGE2 in vitro remains to be elucidated. Some indirect mechanisms, such as stimulation of gastric mucosal blood flow, are ruled out by these experiments.
从健康志愿者和胃溃疡患者的胃底、胃窦和十二指肠上部区域进行内镜活检，并在含95%氧气和5%二氧化碳的饱和缓冲199培养基中于37摄氏度下孵育。以氚标记的胸腺嘧啶核苷掺入组织DNA来估计DNA合成速率，以此作为细胞完整性的指标。在30分钟的孵育过程中，乙醇（25% v/v）显著（p<0.01）抑制正常受试者胃十二指肠黏膜中的DNA合成约50%，在胃溃疡患者的胃黏膜中甚至抑制三分之二。前列腺素E2（PGE2）本身（1mg/50ml）对DNA合成没有刺激作用；然而，当与乙醇同时给药时，它确实减少了由于乙醇导致的DNA合成的急剧下降（p<0.005）。PGE2在体外细胞保护作用的基本机制仍有待阐明。这些实验排除了一些间接机制，如刺激胃黏膜血流。
