Biemond P, Han H, Swaak A J, Koster J F
Department of Biochemistry I, Medical Faculty, Erasmus University Rotterdam, The Netherlands.
Scand J Rheumatol. 1990;19(2):151-6. doi: 10.3109/03009749009102119.
Superoxide production by polymorphonuclear leukocytes (PMNs) and macrophages was inhibited by piroxicam and other non-steroidal anti-inflammatory drugs both in vitro and in vivo. Hitherto, data have only been available on blood PMNs and macrophages. In order to investigate the situation in the joint, PMNs were isolated from synovial fluid before and after 24 h of piroxicam treatment in patients with rheumatoid arthritis. Isolated PMNs were stimulated with PMA and serum-treated zymosan. The capacity of synovial fluid PMNs to produce superoxide decreased by 30% after piroxicam treatment. A similar decrease was found for blood PMNs. No difference in superoxide production was found between blood PMNs and synovial fluid PMNs which were obtained simultaneously. From the fact that the piroxicam concentration in synovial fluid was 40% of the serum value, it can be concluded that piroxicam probably became bound to PMNs before they entered the joint cavity. These results indicate that at the site of the inflammation the superoxide production by PMNs is inhibited by piroxicam treatment. The inhibition of superoxide production is probably important in the effect of piroxicam and other non-steroidal anti-inflammatory drugs in rheumatoid arthritis.
吡罗昔康和其他非甾体抗炎药在体外和体内均可抑制多形核白细胞(PMN)和巨噬细胞产生超氧化物。迄今为止,仅有关于血液中PMN和巨噬细胞的数据。为了研究关节内的情况,从类风湿性关节炎患者接受吡罗昔康治疗24小时前后的滑液中分离出PMN。用佛波酯(PMA)和经血清处理的酵母聚糖刺激分离出的PMN。吡罗昔康治疗后,滑液PMN产生超氧化物的能力下降了30%。血液中的PMN也有类似程度的下降。同时获取的血液PMN和滑液PMN之间在超氧化物产生方面未发现差异。鉴于滑液中吡罗昔康的浓度为血清值的40%,可以得出结论,吡罗昔康可能在PMN进入关节腔之前就已与它们结合。这些结果表明,在炎症部位,吡罗昔康治疗可抑制PMN产生超氧化物。超氧化物产生的抑制可能在吡罗昔康和其他非甾体抗炎药对类风湿性关节炎的作用中起重要作用。