NADPH氧化酶在糖尿病肾病中的作用

Role of NADPH oxidase in the diabetic nephropathy

还原型烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶是许多非吞噬细胞中活性氧簇(ROS)产生的主要来源。在高血糖、高血脂、血管紧张素Ⅱ及各种细胞因子、生长因子的作用下,NADPH氧化酶被激活,发生呼吸链级联反应,产生过量的ROS,参与氧化应激,并作为氧化应激的中心环节,通过形成晚期糖基化终末产物(AGE)、激活蛋白激酶C(PKC)、转录因子如核因子(NF)-кB等途径,改变肾脏血液动力学,影响细胞外基质的重构,激活细胞内信号转导等,促进糖尿病肾病的发生发展。调节NADPH氧化酶的活性以抑制肾脏的氧化应激,有望成为延缓肾功能损害的有效治疗措施。

Nicotinamide adenine dinucleotide phosphate （NADPH） oxidase is a major source of reactive oxygen species （ROS） produced in many nonphagocytic cells. Response to the stimulus such as hyperglycemia, hyperlipidemia, angiotensin Ⅱ and various kinds of cytokines and growth factors, NADPH oxidase could be activated, and produce excessive ROS through the respiratory chain. As a central part of the oxidative stress, ROS plays an important role in heamodynamics, matrix reconstitution, tubulointerstitial fibrosis and signal transduction by increasing the advanced glyeation end product （AGE） formation, aetivating the protein kinase C（PKC） and transcription factors such as nuclear factor（ NF）-κB pathways in diabetic kidney. Modulation of this enzymatic complex could be a promising step to prevent oxidative stress occurred in renal dysfunction.