Gao Jun-Peng, Sun Shan, Li Wen-Wei, Zhao Hong, Cai Ding-Fang
Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Sheng Li Ke Xue Jin Zhan. 2008 Jul;39(3):214-20.
Cyclooxygenase (COX) is the major target of non-steroidal anti-inflammatory drugs (NSAIDs). Since its discovery in the early 1990s, COX has been identified as a major player in inflammatory reactions. "neuroinflammation" is triggered and sustained by activation of resident cells, particularly microglia. Intensive researches have been made in the last decade concerning the COX pathway and its effect on microglial activation as well as other processes involved in neurondegeneration. This article reviewed new data in this area, focusing on three major neurodegenerative diseases, Alzheimer's disease (AD), Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS). By highlighting current knowledge in this field, it may reveal novel insight into disease mechanisms and help to design better therapies for these disorders.
环氧化酶（COX）是非甾体抗炎药（NSAIDs）的主要作用靶点。自20世纪90年代初被发现以来，COX已被确定为炎症反应中的主要参与者。“神经炎症”由驻留细胞，特别是小胶质细胞的激活引发并持续存在。在过去十年中，针对COX途径及其对小胶质细胞激活以及神经退行性变中其他相关过程的影响进行了深入研究。本文综述了该领域的新数据，重点关注三种主要的神经退行性疾病，即阿尔茨海默病（AD）、帕金森病（PD）和肌萎缩侧索硬化症（ALS）。通过强调该领域的现有知识，可能会揭示疾病机制的新见解，并有助于为这些疾病设计更好的治疗方法。
