Ahnfelt-Rønne I, Nielsen O H
Agents Actions. 1987 Jun;21(1-2):191-4. doi: 10.1007/BF01974941.
Using a novel spectrophotometric assay to detect free radical scavengers, the effects of sulfasalazine, a compound frequently administered in the treatment of chronic inflammatory bowel disease, and its main metabolites, 5-aminosalicylic acid (5-ASA), sulfapyridine, and N-acetyl-5-ASA, were compared with biological antioxidants (nordihydroguaiaretic acid (NDGA), alpha-tocopherol, and ascorbic acid) and antiinflammatory salicylates (acetylsalicylic acid and sodium salicylate). The results show that 5-ASA, but neither sulfasalazine and its other metabolites, nor the salicylates, shares with the biological antioxidants the property of being a potent scavenger of free radicals. Since 5-ASA is formed in millimolar concentrations in the colon of sulfasalazine-treated patients this mode of action may explain the beneficial effect of sulfasalazine in inflammatory bowel disease. Locally formed 5-ASA may break the free radical chain reaction initiated and maintained by activated phagocytes, thus arresting the perpetuating tissue destruction. This mechanism may indicate a general potential for radical scavengers in chronic inflammation.
使用一种新型分光光度法检测自由基清除剂，比较了柳氮磺胺吡啶（一种常用于治疗慢性炎症性肠病的化合物）及其主要代谢产物5-氨基水杨酸（5-ASA）、磺胺吡啶和N-乙酰-5-ASA与生物抗氧化剂（去甲二氢愈创木酸（NDGA）、α-生育酚和抗坏血酸）以及抗炎性水杨酸盐（乙酰水杨酸和水杨酸钠）的效果。结果表明，5-ASA与生物抗氧化剂一样，是一种有效的自由基清除剂，而柳氮磺胺吡啶及其其他代谢产物以及水杨酸盐均不是。由于在接受柳氮磺胺吡啶治疗的患者结肠中会以毫摩尔浓度形成5-ASA，这种作用方式可能解释了柳氮磺胺吡啶在炎症性肠病中的有益作用。局部形成的5-ASA可能会中断由活化吞噬细胞引发和维持的自由基链反应，从而阻止持续的组织破坏。这种机制可能表明自由基清除剂在慢性炎症中具有普遍的作用潜力。
