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抗坏血酸与糖尿病肾病

Ascorbic Acid and Diabetic Nephropathy
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摘要 糖尿病肾病发病机制复杂,目前认为氧化应激在其发生、发展过程中起重要作用。高血糖和胰岛素抵抗都可导致糖尿病患者体内氧化应激水平增加,而肾组织对氧化应激尤为敏感。氧化应激可通过引起早期肾小球血流动力学改变、肾组织内细胞外基质重构及肾组织炎性反应等途径对肾脏造成损伤。抗坏血酸是体内最重要的水溶性抗氧化剂,它能使活性氧簇清除增加、生成减少,并抑制活性氧簇介导的信号通路和转录因子的活化,减轻氧化应激的发生、发展;另外,抗坏血酸还有改善胰岛素敏感性、调节免疫、增强抗氧化酶活性等作用,从而能有效保护肾脏功能,延缓其病程,有望成为该疾病的辅助治疗手段。 The pathogenesis of diabetic nephropathy is complicated, currently oxidative stress is speculated to play a crucial role in the initiation and progression of diabetic nephropathy. Hyperglycacmia and insulin resistance will increase the level of oxidative stress in diabetic patient, furthermore kidney is especially sensitive to oxidative stress. Oxidative stress will damage the function of kidney by causing early change of glomerular hemedynamics, reconstruction of extracellular matrix and inflammatory reaction in kidney. Ascorblc acid is the most important hydrosoluble antioxidant in human body, which not only can enhance the elimination as well as reduce the production of reactive oxygen species, but also inhibit the activation of reactive oxygen species mediated signal pathways and transcriptional factors, therefore can relieve the initiation and progression of oxidative stress ; moreover ascorbic acid has the effect of improving insulin sensitivity, immunoregnlation and enhancing the activity of antioxidant enzymes, which thereby could protect the renal function, and improve diabetic nephropathy,thus render it as a promising adjuvant therapy for diabetic nephropathy.
出处 《医学综述》 2007年第19期1493-1495,共3页 Medical Recapitulate
关键词 糖尿病肾病 抗坏血酸 氧化应激 活性氧簇 Diabetic nephropathy Ascorbic acid Oxidative stress Reactive oxygen species
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参考文献19

  • 1Li JM,Shan AM.ROS generation by nonphagocytic NADPH oxidase:potential relevance in diabetic nephropathy[J].J Am Soc Nephrol,2003,14(8 Suppl 3):S221-226.
  • 2Kitada M,Koya D,Sugimoto T,et al.Translocation of glomerular p47phox and p67phox by protein kinase C-beta activation is required for oxidative stress in diabetic nephropathy[J].Diabetes,2003,52(10):2603-2614.
  • 3Groop PH,Forsblom C,Thomas MC.Mechanisms of disease:pathway-selective insulin resistance and microvascular complications of diabetes[J].Nat Clin Pract Endocrinol Metab,2005,1(2):100-110.
  • 4Obrosova IG,Fathallah L,Liu E,et al.Early oxidative stress in the diabetic kidney:effect of DL-alpha-lipoic acid[J].Free Radic Biol Med,2003,34(2):186-195.
  • 5Chen L,Jia RH,Qiu CJ,et al.Hyperglycemia inhibits the uptake of dehydroascorbate in tubular epithelial cell[J].Am J Nephrol,2005,25(5):459-465.
  • 6Fukami K,Ueda S,Yamagishi S,et al.AGEs activate mesangial TGF-beta-Smad signaling via an angiotensin Ⅱ type I receptor interaction[J].Kidney Int,2004,66(6):2137-2147.
  • 7Lee HB,Yu MR,Yang Y,et al.Reactive oxygen species-regulated signaling pathways in diabetic nephropathy[J].J Am Soc Nephrol,2003,14(8 Suppl 3):S241-S245.
  • 8Lee EA,Seo JY,Jiang Z,et al.Reactive oxygen species mediate high glucose-induced plasminogen activator inhibitor-1 up-regulation in mesangial cells and in diabetic kidney[J].Kidney Int,2005,67(5):1762-1771.
  • 9Ha H,Yu MR,Choi YJ,et al.Role of high glucose-induced nuclear factor-kappaB activation in monocyte chemoattractant protein-1 expression by mesangial cells[J].J Am Soc Nephrol,2002,13(4):894-902.
  • 10Morii T,Fujita H,Narita T,et al.Association of monocyte chemoattractant protein-1 with renal tubular damage in diabetic nephropathy[J].J Diabetes Complications,2003,17(1):11-15.

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