Cuperus R A, Muijsers A O, Wever R
Arthritis Rheum. 1985 Nov;28(11):1228-33. doi: 10.1002/art.1780281106.
We investigated the effect of antiarthritic drugs containing thiol groups, such as D-penicillamine, tiopronin (N-[2-mercaptopropionyl]glycine), sodium aurothiomalate, and aurothioglucose, on the chlorinating activity of myeloperoxidase purified from human leukocytes. Hypochlorite, the reactive product of the reaction catalyzed by myeloperoxidase, was effectively scavenged by these antiarthritic drugs, and in addition, D-penicillamine and tiopronin inhibited myeloperoxidase itself. The above-mentioned effects of these drugs were observed at concentrations that occur in the serum of rheumatoid arthritis patients treated with these agents. We suggest that the therapeutic effect of these antiarthritic drugs may be due to the protection of tissues against the reactive HOCI released by activated granulocytes at inflamed sites.
我们研究了含巯基的抗关节炎药物，如D-青霉胺、硫普罗宁（N-[2-巯基丙酰基]甘氨酸）、金硫代苹果酸钠和金硫葡萄糖，对从人白细胞中纯化的髓过氧化物酶氯化活性的影响。髓过氧化物酶催化反应的活性产物次氯酸盐可被这些抗关节炎药物有效清除，此外，D-青霉胺和硫普罗宁还可抑制髓过氧化物酶本身。在接受这些药物治疗的类风湿性关节炎患者血清中出现的浓度下可观察到这些药物的上述作用。我们认为这些抗关节炎药物的治疗作用可能是由于保护组织免受炎症部位活化粒细胞释放的活性次氯酸的损伤。
