Lambat Z, Conrad N, Anoopkumar-Dukie S, Walker R B, Daya S
Faculty of Pharmacy, Rhodes University, Grahamstown, South Africa.
Metab Brain Dis. 2000 Dec;15(4):249-56. doi: 10.1023/a:1011115006856.
There is increasing evidence suggesting a protective role for anti-inflammatory medications in neurological disorders such as Alzheimer's disease (AD). While there has not been any direct evidence for this, a number of clinical studies indicate that those patients who have had a history of nonsteroidal anti-inflammatory use, have a lower incidence of AD. Since there is currently no evidence on the mechanism by which these agents offer possible neuroprotection, we investigated the potential neuroprotective properties of the nonsteroidal anti-inflammatory drug, ibuprofen, by examining whether this agent could reduce lipid peroxidation and superoxide radical generation. Quinolinic acid and cyanide, known neurotoxins, were used to induce lipid peroxidation and superoxide anion formation respectively, in rat brain homogenate. The results show that ibuprofen significantly (p<0.05) reduced quinolinic acid-induced lipid peroxidation and cyanide-induced superoxide production. The results of the present report therefore suggest a possible mechanism for the neuroprotective effect of ibuprofen.
越来越多的证据表明,抗炎药物在诸如阿尔茨海默病(AD)等神经疾病中具有保护作用。虽然目前尚无直接证据支持这一点,但多项临床研究表明,有非甾体抗炎药使用史的患者患AD的发病率较低。由于目前尚无证据表明这些药物提供潜在神经保护作用的机制,我们通过研究布洛芬这种非甾体抗炎药是否能减少脂质过氧化和超氧自由基的产生,来探究其潜在的神经保护特性。分别使用已知的神经毒素喹啉酸和氰化物在大鼠脑匀浆中诱导脂质过氧化和超氧阴离子形成。结果表明,布洛芬显著(p<0.05)降低了喹啉酸诱导的脂质过氧化和氰化物诱导的超氧产生。因此,本报告的结果提示了布洛芬神经保护作用的一种可能机制。