N-Acetylcysteine enhances the action of anti-inflammatory drugs as suppressors of prostaglandin production in monocytes
N-Acetylcysteine enhances the action of anti-inflammatory drugs as suppressors of prostaglandin production in monocytes
复制标题
DOI：
10.1080/09629350210000015737
复制
发表时间：
2002-10-01
影响因子：
4.6
通讯作者：
Nahir, AM
中科院分区：
文献类型：
--
作者：
Hoffer, E;Baum, Y;Nahir, AM
非甾体类抗炎药 (NSAID) 的抗炎作用与抑制环氧合酶 (COX) 相关，环氧合酶是负责合成前列腺素的限速酶。由于氧自由基可以充当第二细胞信使，特别是调节花生四烯酸和前列腺素束的代谢，因此抗氧化剂可能会影响活化细胞产生前列腺素似乎是合理的。本研究的重点是抗氧化剂 N-乙酰半胱氨酸 (NAC) 对特异性和非特异性 COX 抑制剂抑制活化单核细胞中前列腺素 E-2 形成的影响。我们发现罗非昔布和双氯芬酸（两种非甾体抗炎药）可显着减少脂多糖诱导的前列腺素 E2 形成。在这些药物中添加 NAC 可以增强 NSAID 的作用。这些结果表明，人们可能期望通过与 NAC 同时给药来增强 COX 抑制剂的抗炎作用，或者以较低的药物水平获得相同的抗炎作用。
THE anti-inflammatory effect of non-steroidal anti-inflammatory drugs ( NSAIDs) is associated with inhibition of cyclooxygenase ( COX), the rate-limiting enzyme responsible for the synthesis of prostaglandins. Since oxygen free radicals can act as second cellular messengers, especially to modulate the metabolism of arachidonic acid and the prostaglandin tract, it seems plausible that antioxidants might affect the production of prostaglandin by activated cells. This research is focused on the effect of the antioxidant N-acetylcysteine (NAC) on the inhibition of prostaglandin E-2 formation in activated monocytes by specific and non-specific COX inhibitors. We found that lipopolysaccharide-induced prostaglandin E2 formation was significantly reduced by rofecoxib and by diclofenac, two NSAIDs. Addition of NAC to each of these drugs enhanced the effect of the NSAIDs. These results suggest that one might expect either a potentiation of the anti-inflammatory effect of COX inhibitors by their simultaneous administration with NAC, or obtaining the same anti-inflammatory at lower drug levels.