Angelis-Stoforidis P, Vajda F J, Christophidis N
Department of Geriatric Services, Alfred Hospital, Australia.
Clin Exp Rheumatol. 1998 Nov-Dec;16(6):703-8.
To elucidate the mechanism of action of a wide range of non-steroidal anti-inflammatory drugs (NSAIDs) on the respiratory burst of isolated normal PMNs in buffered saline and plasma.
The oxidative burst of PMN was assessed by luminol enhanced chemiluminescence and myeloperoxidase-mediated iodination. Cells were stimulated by the synthetic tripeptide N-formyl-methionyl-leucyl-phenylalanine (FMLP), serum coated zymosan or the phorbol ester phorbol myristate acetate (PMA).
When using buffered saline as the suspending medium, tenoxicam, piroxicam, ibuprofen, ketoprofen and diclofenac, at concentrations achieved clinically, inhibited both PMA- and FMLP-induced luminol chemiluminescence. Tenoxicam and piroxicam in buffered saline also inhibited the iodination reaction. However, in plasma, which mimics the in vivo situation more closely, the inhibitory effect was markedly reduced. Only tenoxicam and piroxicam were found to cause the inhibition of luminol chemiluminescence at concentrations achieved clinically.
If these study conditions are representative of the in vivo pathological state, the results suggest that only tenoxicam, piroxicam and possibly diclofenac sodium are likely to possess anti-inflammatory properties which are independent from effects on cyclooxygenase.
阐明多种非甾体抗炎药(NSAIDs)对缓冲盐溶液和血浆中分离出的正常中性粒细胞呼吸爆发的作用机制。
通过鲁米诺增强化学发光和髓过氧化物酶介导的碘化反应评估中性粒细胞的氧化爆发。细胞用合成三肽N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸(FMLP)、血清包被的酵母聚糖或佛波酯佛波醇肉豆蔻酸酯乙酸酯(PMA)刺激。
以缓冲盐溶液作为悬浮介质时,在临床达到的浓度下,替诺昔康、吡罗昔康、布洛芬、酮洛芬和双氯芬酸抑制PMA和FMLP诱导的鲁米诺化学发光。缓冲盐溶液中的替诺昔康和吡罗昔康也抑制碘化反应。然而,在更接近体内情况的血浆中,抑制作用明显降低。仅发现替诺昔康和吡罗昔康在临床达到的浓度下可抑制鲁米诺化学发光。
如果这些研究条件代表体内病理状态,结果表明只有替诺昔康、吡罗昔康以及可能的双氯芬酸钠可能具有独立于对环氧化酶作用的抗炎特性。