聚腺苷二磷酸核糖聚合酶(PARP)可能是糖尿病周围神经病变(DPN)发病机制中的关键触发酶,通过氧化应激等途径导致DPN发生。PARP在DNA修复、基因表达、细胞周期和长期记忆等生物功能方面均发挥重要作用。一旦PARP过度激活,可诱导细胞死亡、抑制糖酵解、大量消耗ATP、促进炎性反应、增加氧氮自由基离子形成和介导氧化应激,引发DPN。本文就PARP、氧化应激等因素在DPN中的作用作一阐述。 Polyadenosine diphosphate ribose polymerase (PARP) may be the key trigger enzyme in the pathogenesis of diabetic peripheral neuropathy (DPN), leading to DPN through oxidative stress and other pathways. PARP plays an important role in biological functions such as DNA repair, gene expression, cell cycle and long-term memory. Once PARP is over-activated, it induces cell death, inhibits glycolysis, consumes ATP in large amounts, promotes inflammatory reactions, increases oxygen and nitrogen free radical ion formation and mediates oxidative stress, triggering DPN. This article describes the role of PARP, oxidative stress and other factors in DPN.