KETOTIFEN EFFECTIVELY PREVENTS MUCOSAL DAMAGE IN EXPERIMENTAL COLITIS
KETOTIFEN EFFECTIVELY PREVENTS MUCOSAL DAMAGE IN EXPERIMENTAL COLITIS
复制标题
DOI：
10.1136/gut.33.11.1498
复制
发表时间：
1992-11-01
期刊：
影响因子：
24.5
通讯作者：
RACHMILEWITZ, D
中科院分区：
文献类型：
--
作者：
ELIAKIM, R;KARMELI, F;RACHMILEWITZ, D
研究人员检查了酮替芬（一种“肥大细胞稳定剂”）对两种实验性结肠炎模型的影响。三硝基苯磺酸或乙酸引起的炎症反应导致结肠合成血小板活化因子、前列腺素E2、血栓素B2、白三烯B4和C4以及髓过氧化物酶活性增加。在诱导结肠炎前 48 小时以及整个实验期间预防性给予酮替芬 100 杯/100 克，每天两次，可显着减少粘膜损伤。这种效应在两种模型中都是一致的，并且伴随着血小板活化因子、前列腺素E2、血栓素B2以及白三烯C4和B4的粘膜生成的显着减少。髓过氧化物酶活性也降低，仅在乙酸模型中达到显着水平。这项研究表明，酮替芬可以在药理上控制三硝基苯磺酸和醋酸结肠炎。酮替芬的作用机制尚未确定。酮替芬在治疗活动性炎症性肠病或预防病情加重或两者方面的潜力仍有待阐明。
The effects of ketotifen, a 'mast cell stabiliser,' on two models of experimental colitis were examined. The inflammatory response elicited by either trinitrobenzene sulphonic acid or acetic acid resulted in increased colonic synthesis of platelet activating factor, prostaglandin E2, thromboxane B2, leukotrienes B4 and C4, and myeloperoxidase activity. Intragastric administration of ketotifen 100 mug/100 g twice daily significantly decreased mucosal damage when given prophylactically 48 hours before the induction of colitis and then throughout the experiment. This effect was consistent in both models and was accompanied by a significant reduction in mucosal generation of platelet activating factor, prostaglandin E2, thromboxane B2, and leukotrienes C4 and B4. Myeloperoxidase activity was reduced as well, reaching significance only in the acetic acid model. This study shows that both trinitrobenzene sulphonic acid and acetic acid colitis can be pharmacologically manipulated by ketotifen. The mechanism of action of ketotifen has not yet been determined. Ketotifen's potential in the treatment of active inflammatory bowel disease or in the prevention of exacertations, or both, remains to be elucidated.