Rachmilewitz D, Karmeli F, Eliakim R
Dept. of Gastroenterology, Hadassah University Hospital, Jerusalem, Israel.
Scand J Gastroenterol Suppl. 1990;172:19-21. doi: 10.3109/00365529009091904.
Release of platelet-activating factor (PAF) by cultured colonic mucosa of patients with ulcerative colitis and healthy controls was determined. Before stimulation with calcium ionophore or antihuman IgE, no PAF release by control mucosa and minimal PAF release by mucosa of the colitis patients were detected. After stimulation with calcium ionophore, PAF release was four to five times higher by colonic mucosa of the colitis patients than of the controls. After stimulation with antihuman IgE, PAF release was twice as high by colonic mucosa of colitis patients as by control mucosa. Prednisolone, sulphasalazine, and mesalazine inhibited PAF activity stimulated by calcium ionophore in a dose-dependent manner. The results suggest that the use of PAF antagonists in the treatment of ulcerative colitis should be investigated.
测定了溃疡性结肠炎患者和健康对照者培养的结肠黏膜中血小板活化因子(PAF)的释放情况。在用钙离子载体或抗人IgE刺激之前,未检测到对照黏膜释放PAF,而结肠炎患者的黏膜释放的PAF极少。在用钙离子载体刺激后,结肠炎患者的结肠黏膜释放的PAF比对照组高4至5倍。在用抗人IgE刺激后,结肠炎患者的结肠黏膜释放的PAF是对照黏膜的两倍。泼尼松龙、柳氮磺胺吡啶和美沙拉嗪以剂量依赖的方式抑制钙离子载体刺激的PAF活性。结果表明,应研究PAF拮抗剂在溃疡性结肠炎治疗中的应用。