血管内皮细胞生长因子-一氧化氮轴与糖尿病肾病

Vascular endothelial growth factor-nitric oxide axis and diabetic nephropathy

血管内皮生长因子（VEGF）-一氧化氮（NO）耦联被称为VEGF-NO轴,其对维持肾小球血管内皮细胞功能起重要作用,其解耦联可能参与糖尿病肾病的发生、发展.内皮型一氧化氮合酶（eNOS）活性降低可能是糖尿病肾脏VEGF-NO轴解耦联的关键环节.肥胖、高脂血症以及氧化应激是导致糖尿病肾脏VEGF-NO轴解耦联的重要原因.脂联素、血红素加氧酶-1明显改善糖尿病大鼠肾小球血管内皮细胞的功能、降低白蛋白尿,其机制可能是通过抗氧化应激作用改善VEGF-NO轴的功能.

The coupling of vascular endothelial growth factor （VEGF） with nitric oxide （NO）,known as the VEGF-NO axis,plays a critical role in maintaining normal glomerular endothelial cell function,its uncoupling involves in the occurrence and development of diabetic nephropathy.Reduction of endothelial nitric oxide synthase （eNOS） activity is likely to be the key mechanism of VEGF-NO axial decoupling in diabetic kidney.Obesity,hyperlipidemia,and oxidative stress may be main reasons of VEGF-NO axis uncoupling in diabetes kidney.Adiponectin,heme oxygenase-1 could obviously improve glomerular endothelial cell function of diabetic rat,reduce proteinuria via resisting oxidative stress to improve the function of the VEGF-NO axis.