尼克酰胺腺嘌呤二核苷酸磷酸氧化酶在血管性认知障碍中的作用及其机制的研究进展

The role of nicotinamide adenine dinucleotide phosphate oxidase in vascular cognitive impairment and its mechanism:a research progress

氧化应激(OS)是导致血管性认知障碍(VCI)的因素之一。尼克酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶(NOX)产生的活性氧(ROS)是VCI重要的致病分子。VCI的危险因素如高血糖及缺血/再灌注等在上游增加NOX的活化;其他危险因素如高龄、高血压及卒中是NOX依赖ROS产生的下游损伤。VCI的成因包括与NOX相关的危险因素及NOX依赖的ROS导致的细胞损伤。研究表明,抑制NOX活性可减轻认知障碍、降低其发生的危险因素。本文对NOX在VCI中的作用及其机制的研究进展进行综述。

Oxidative stress(OS)is one of the factors leading to vascular cognitive impairment(VCI).Reactive oxygen species(ROS)produced by Nicotinamide adenine dinucleotide phosphate oxidase(NOX)is an important pathogenic molecule of VCI.Risk factors for VCI such as hyperglycemia and decomposition/re-implantation always increases an upstream NOX activation.Other risk factors such as advanced age,hypertension and stroke are the downstream damage caused by NOX-dependent ROS.The causes of VCI include both risk factors related to NOX and the cell damage caused by NOX-dependent ROS.Studies have shown that the inhibiting of NOX activity can reduce cognitive impairment and the risk factors in animal models of VCI.In this article,we review the research progress of the role and mechanism of NOX in VCI.