McCafferty D M, Zeitlin I J
Department of Physiology and Pharmacology, University of Strathclyde, Glasgow, Scotland.
Agents Actions. 1992;Spec No:C79-81.
A standard colitic lesion was induced in male BKA mice by intrarectal administration of butyric acid (7.5%, 0.1 ml, 10 sec contact). Animals were killed after 5 h and the 'colitic score', increase in colonic tissue water ('oedema') and colonic tissue content of myeloperoxidase (MPO, a marker for neutrophils) were determined. Drug was administered intrarectally in 0.2 ml saline 20 min before colitis induction. In colitic animals given vehicle alone, all these parameters increased (P less than 0.05) compared to the non-colitic controls. In colitic animals given 16,16-dimethyl PGE2 (0.2-20000 micrograms/kg), colitic score was reduced (P less than 0.05) at all dose levels when compared with vehicle-treated colitic animals. The oedema and MPO showed a dose-related reduction (r = -0.895 and -0.904 respectively). In mouse colon 16,16-dimethyl PGE2 showed a protective action against butyric acid-induced colitic damage.
通过直肠内给予丁酸(7.5%,0.1 ml,接触10秒)在雄性BKA小鼠中诱导出标准的结肠炎病变。5小时后处死动物,测定“结肠炎评分”、结肠组织水分增加量(“水肿”)和结肠组织髓过氧化物酶(MPO,中性粒细胞标志物)含量。在诱导结肠炎前20分钟,将药物以0.2 ml生理盐水经直肠给药。与未患结肠炎的对照组相比,仅给予赋形剂的结肠炎动物的所有这些参数均增加(P<0.05)。与给予赋形剂治疗的结肠炎动物相比,给予16,16-二甲基前列腺素E2(0.2 - 20000微克/千克)的结肠炎动物在所有剂量水平下结肠炎评分均降低(P<0.05)。水肿和MPO呈现剂量相关的降低(分别为r = -0.895和 -0.904)。在小鼠结肠中,16,16-二甲基前列腺素E2对丁酸诱导的结肠损伤具有保护作用。