Peskar B M, Dreyling K W, Peskar B A, May B, Goebell H
Agents Actions. 1986 Jun;18(3-4):381-3. doi: 10.1007/BF01965001.
Release of sulfidopeptide (SP)-leukotrienes (LT) in vitro from normal human colonic mucosa and from mucosal tissue obtained from patients with Crohn's disease (CD) and ulcerative colitis (UC) was investigated. It was found that inflamed mucosal tissue released significantly more SP-LT than normal colonic mucosa both under control conditions and after addition of calcium ionophore A23187. These results indicate the presence of endogenous stimuli as well as an increased responsiveness to an exogenous stimulus of LT formation in the inflamed mucosa. Sulfasalazine (SASP), a drug used in inflammatory bowel diseases, and its active metabolite 5-aminosalicylic acid (5-ASA) were found to inhibit colonic mucosal SP-LT formation, while only 5-ASA inhibited simultaneously synthesis of another arachidonic acid-derived inflammatory mediator, prostaglandin (PG) E2. The results suggest that SP-LT might be important mediators of inflammation in CD and UC.
研究了正常人结肠黏膜以及克罗恩病（CD）和溃疡性结肠炎（UC）患者的黏膜组织在体外释放硫化肽（SP）-白三烯（LT）的情况。结果发现，无论是在对照条件下还是添加钙离子载体A23187后，发炎的黏膜组织释放的SP-LT均显著多于正常结肠黏膜。这些结果表明，发炎黏膜中存在内源性刺激，并且对LT形成的外源性刺激反应性增强。发现用于炎症性肠病的药物柳氮磺胺吡啶（SASP）及其活性代谢物5-氨基水杨酸（5-ASA）可抑制结肠黏膜SP-LT的形成，而只有5-ASA同时抑制另一种花生四烯酸衍生的炎症介质前列腺素（PG）E2的合成。结果表明，SP-LT可能是CD和UC炎症的重要介质。
