缺血性脑血管疾病治疗的抗氧化应激策略

自由基是细胞呼吸及正常代谢过程中产生的高活性分子 ,氧化应激 (OS)是细胞内自由基生成和清除能力失衡 ,是缺血性脑血管疾病重要病理反应过程。缺血性脑损伤后 ,活性氧自由基 (ROS)增加 ,以不同的细胞分子机制引起组织损伤。自由基可以损伤细胞内脂质、蛋白质、核酸等重要物质 ,继而通过坏死或凋亡的方式引起细胞死亡。抗氧化剂可防止脑组织损伤 ,改善神经细胞存活率及功能。本文就治疗缺血性脑血管疾病的抗氧化剂作一综述 ,并分析动物与临床试验结果不一致的原因 ,提出缺血性脑血管疾病治疗的抗氧化应激策略。

Strategies against oxidative stress for therapy of ischemic cerebrovascular diseases

Free radicals are highly reactive molecules generated predominantly during cellular respiration and normal metabolism. Imbalance between cellular production of free radicals and the ability of cells to defend against them is referred to oxidative stress (OS). OS has been implicated as a potential contributor to the pathogenesis of ischemic cerebrovascular diseases. After brain injury by ischemia, the production of reactive oxygen species (ROS) may increase, leading to tissues damage via several different cellular molecular pathways. Radicals can cause damage to cardinal cellular components such as lipids, proteins, and neucleic acids, leading to subsequent cell death by modes of necrosis or apoptosis. Treatment with antioxidants may prevent propagation of tissues damage and improve both the survival and neurological outcome. The present paper reviews the antioxidants therapy in ischemic cerebrovascular disease, discusses probable reasons of inconsistency between animal experiments and clinical trials on antioxidants, and puts forward strategies against oxidative stress in the treatment of ischemic cerebrovascular diseases.