Asanuma M, Miyazaki I, Ogawa N
Department of Brain Science, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikatacho, Okayama 700-8558, Japan.
Curr Pharm Des. 2004;10(6):695-700. doi: 10.2174/1381612043453072.
It is well known that nonsteroidal anti-inflammatory drugs (NSAIDs) possess anti-inflammatory, analgesic and antipyretic properties by inhibiting cyclooxygenase (COX), a prostaglandin-synthesizing enzyme. It has also been revealed that NSAIDs exert inhibitory effects on the generating system of nitric oxide radicals and modulating effects on transcription factors which are related to inflammatory reactions including cytokine expression. Recently, a number of studies have been conducted focusing on the neuroprotective effects of NSAIDs, since it has been reported that inflammatory processes are associated with the pathogenesis of several neurodegenerative diseases including Alzheimer's disease and Parkinson's disease. In the experimental model of Parkinson's disease, NSAIDs have also exerted neuroprotective effects which are based not only on their COX-inhibiting effects but also on other properties: inhibitory effects on nitric oxide synthesis, action as agonists for peroxisome proliferator-activated receptor gamma, and some unknown pharmacological effects. In this article, various pharmacological effects of NSAIDs except their inhibitory action on COX are reviewed, and possible neuroprotective effects of NSAIDs have been discussed on neurodegenerative diseases, especially Parkinson's disease.
众所周知，非甾体抗炎药（NSAIDs）通过抑制环氧化酶（COX，一种前列腺素合成酶）具有抗炎、镇痛和解热特性。还发现NSAIDs对一氧化氮自由基生成系统具有抑制作用，并对与包括细胞因子表达在内的炎症反应相关的转录因子具有调节作用。最近，由于有报道称炎症过程与包括阿尔茨海默病和帕金森病在内的几种神经退行性疾病的发病机制有关，因此已经开展了许多关于NSAIDs神经保护作用的研究。在帕金森病的实验模型中，NSAIDs也发挥了神经保护作用，这不仅基于它们对COX的抑制作用，还基于其他特性：对一氧化氮合成的抑制作用、作为过氧化物酶体增殖物激活受体γ激动剂的作用以及一些未知的药理作用。在本文中，综述了NSAIDs除对COX抑制作用之外的各种药理作用，并讨论了NSAIDs对神经退行性疾病，尤其是帕金森病可能的神经保护作用。
