聚腺苷二磷酸核糖聚合酶、离子通道和自身免疫与糖尿病周围神经病变的研究进展

摘要

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。%[Summary] Poly adenosine diphosphate (ADP) ribose polymerase (PARP) may act as a key trigger enzyme in the pathogenesis of diabetic peripheral neuropathy (DPN). PARP may play an important role in the development of DPN through a variety of mechanisms linking with DNA repair ,gene expression ,cell cycle ,long‐term memory and other biological processes. The excessive activation of PARP can induce cell death ,inhibition of glycolysis ,consumption of ATP ,response to inflammation ,formation of oxygen ions and oxidative stress. This article reviewed the relationship of PARP and oxidative stress and DPN.