Gilbertson T J, Ruwart M J, Stryd R P, Brunden M N, Friedle N M, Rush B D, Christianson C A
Prostaglandins. 1983 Nov;26(5):745-59. doi: 10.1016/0090-6980(83)90059-x.
Oral and subcutaneous administration of 16,16-dimethylprostaglandin E2 (16,16-dimethyl PGE2) resulted in an increase in the dry weight of the stomach and small intestine of the female rat. This weight response was rapid, controlled rather than continuously progressing, dose dependent and reversible. The dry weight of the colon also increased but this was not studied in detail. Two-day treatment with 16,16-dimethyl PGE2 caused an increase in the incorporation of 3H-thymidine into the duodenum, jejunum and colon suggesting an increase in cell number. Incorporation into the stomach and ileum was not changed. The number of goblet cells per crypt was increased by prostaglandin treatment in all parts of the small intestine. Since these are mucus producing cells, the small intestine may have increased in cell number and mucus production. Both anti-secretory and cytoprotective doses of 16,16-dimethyl PGE2 caused weight increases in the stomach and small intestine. However, the weight gain by itself was not sufficient to protect the stomach or small intestine from necrotic agents after the prostaglandin was discontinued.
口服和皮下注射16,16 - 二甲基前列腺素E2(16,16 - 二甲基PGE2)可导致雌性大鼠胃和小肠干重增加。这种重量反应迅速,是可控的而非持续进展,具有剂量依赖性且可逆。结肠干重也增加,但未对此进行详细研究。用16,16 - 二甲基PGE2进行为期两天的治疗可使3H - 胸腺嘧啶核苷掺入十二指肠、空肠和结肠增加,提示细胞数量增加。掺入胃和回肠的情况未发生变化。前列腺素处理使小肠各部位每个隐窝的杯状细胞数量增加。由于这些是产生黏液的细胞,小肠的细胞数量和黏液分泌量可能增加。16,16 - 二甲基PGE2的抗分泌剂量和细胞保护剂量均可导致胃和小肠重量增加。然而,在停用前列腺素后,体重增加本身并不足以保护胃或小肠免受坏死因子的影响。