Chiarugi Alberto
Department of Pharmacology, University of Florence, Viale Pieraccini 6, 50139 Firenze, Italy.
Pharmacol Res. 2005 Jul;52(1):15-24. doi: 10.1016/j.phrs.2005.02.018.
Over the past decade, poly(ADP-ribosyl)ation has emerged as a crucial event in the pathogenesis of ischemic stroke. A large body of evidence unambiguously demonstrates that activity of poly(ADP-ribose) polymerase-1 (PARP-1) significantly increases during brain ischemia, and that inhibition of this enzymatic activity affords substantial neuroprotection from ischemic brain injury. This review strictly focuses on literature on poly(ADP-ribosyl)ation and ischemic stroke, highlighting the pathogenetic role of poly(ADP-ribose) in ischemic neuronal death, and the therapeutic relevance of drugs modulating its metabolism to pharmacological treatment of cerebral ischemia.
在过去十年中，多聚（ADP-核糖）化已成为缺血性中风发病机制中的一个关键事件。大量证据明确表明，在脑缺血期间，多聚（ADP-核糖）聚合酶-1（PARP-1）的活性显著增加，并且抑制这种酶活性可从缺血性脑损伤中提供实质性的神经保护作用。本综述严格聚焦于多聚（ADP-核糖）化与缺血性中风的文献，强调多聚（ADP-核糖）在缺血性神经元死亡中的致病作用，以及调节其代谢的药物对脑缺血药物治疗的治疗相关性。
