Iuliano L, Colavita A R, Leo R, Praticò D, Violi F
Institute of Clinical Medicine I, University La Sapienza, Rome, Italy.
Free Radic Biol Med. 1997;22(6):999-1006. doi: 10.1016/s0891-5849(96)00488-1.
This article reviews our current understanding of the role of oxygen free radicals in platelet activation. Several studies have indicated that platelets, in analogy to other circulating blood cells, are able to produce oxygen free radicals, which are likely to play an important role in the mechanism of platelet activation and aggregation. Platelet activation has been obtained with very low, physiologically relevant concentrations of radicals generated chemically, by leukocytes, and by hemoglobin derived from membrane leakage of erythrocytes. Knowledge of the role of reactive species in platelet physiology is relevant because platelets are brought into close contact with other cells capable of producing free radicals, such as neutrophils, macrophages, and endothelial cells, during the formation of thrombus. The physiopatological importance of these findings is high because it is now emerging that free radicals may have a role in the mechanism of atherosclerosis and its thrombotic complications, where the causative role of platelets is well documented. This background suggests therapeutic interventions with antioxidants as antiplatelet agents to improve the pharmacological effect of classical antiplatelet drug such as aspirin.
本文综述了我们目前对氧自由基在血小板活化中作用的理解。多项研究表明，与其他循环血细胞类似，血小板能够产生氧自由基，这些氧自由基可能在血小板活化和聚集机制中发挥重要作用。通过化学方法、白细胞以及红细胞膜渗漏产生的血红蛋白所生成的极低浓度、与生理相关的自由基已能使血小板活化。了解活性物质在血小板生理学中的作用具有重要意义，因为在血栓形成过程中，血小板会与其他能够产生自由基的细胞（如中性粒细胞、巨噬细胞和内皮细胞）密切接触。这些发现具有很高的病理生理学重要性，因为现在越来越清楚自由基可能在动脉粥样硬化及其血栓形成并发症的机制中起作用，而血小板在其中的致病作用已有充分记录。这一背景提示，使用抗氧化剂作为抗血小板药物进行治疗干预，以提高阿司匹林等经典抗血小板药物的药理作用。
