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糖基化终产物对牛视网膜毛细血管周细胞内抗氧化能力的影响 被引量:6

Modification of enzymatic antioxidants in bovine retinal capillary pericytes by advanced glycation end products
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摘要 目的 通过测量糖基化终产物对培养的牛视网膜毛细血管周细胞抗氧化物酶和脂质过氧化物含量的影响 ,以探讨氧化应激在糖尿病视网膜病变进程中的作用。 方法 不同浓度的糖基化终产物(0 ,8,32 ,12 5 ,5 0 0 ,2 0 0 0μg/ ml)与周细胞作用 4 d后 ,以分光光度法测量细胞内过氧化氢酶的活性及过氧化脂质丙二醛的含量。 结果 糖基化终产物能以剂量依赖的方式降低周细胞内过氧化氢酶的活性 (r=- 0 .714 ,P<0 .0 1) ,增加丙二醛的含量 (r=0 .74 8,P<0 .0 1) ,与对照组相比 ,当糖基化终产物浓度达到32 μg/ ml时 ,两者比较差异有显著性的意义 (P<0 .0 1)。 结论 氧化应激的增加可能是早期糖尿病视网膜病变中周细胞丧失的原因之一。 Objective To investigate the effect of advanced glycation end products (AGEs) on the catalase activity and the levels of malondialdehyde in cultured bovine retinal capillary pericytes (BRPs), and to investigate the relationship between oxidative stress and diabetic retinopathy. Methods Cultured BRPs were exposed to AGEs (0, 8, 32, 125, 500, 2 000 μg/ml) for four days. Activity and the levels of catalase and malondialdehyde in cultured BRPs were examined by spectrophotometry. Results AGEs decreased the catalase activity, whereas increased the levels of malondialdehyde of cultured BRPs in a dose dependent manner ( r=-0.714, r=0.748, P< 0.01).There were significant differences between BRPs cultured in 32 μg/ml AGEs and in control group ( P< 0.01), while no significant differences between BRPs cultured in non glycated bovine serum albumin and absence of bovine serum albumin were found. Conclusion Oxidative stress may be one of the reasons why the pericyte disappears in diabetic retinopathy.
出处 《中华眼底病杂志》 CAS CSCD 2002年第2期143-145,共3页 Chinese Journal of Ocular Fundus Diseases
关键词 糖基化终产物 视网膜 毛细血管 抗氧化能力 过氧化氢酶 丙二醛 糖尿病视网膜病变 Pericytes/metabolism Glycosylation end products,advanced Catalase Malondialdehyde Diabetic retinopathy/metabolism
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  • 1于珮,于德民,齐建成,王静,张秋梅,张景云,汤云昭,邢秋玲,李明珍.高糖通过PI3K-Akt信号途径抑制内皮细胞迁移和增殖及血管发生改变[J].中华医学杂志,2006,86(48):3425-3430. 被引量:17
  • 2Simo R, Hemandez C. Intravitreous anti - VEGF for diabetic retinopathy: hopes and fears for a new therapeutic strategy [ J ]. Diabetologia, 2008,51 (9) : 1574 - 1580.
  • 3Cemak M, Markovic O, Cemak A. The treatment of the rubeosis of the iris and the neovascular glaucoma in proliferative diabetic retinopathy by means of anti - VEGF [ J ]. Cesk Slov Oftalmol, 2008,64 (6) :234 -236.
  • 4Huang Q, Sheibani N. High glucose promotes retinal endothelial cell migration through activation of Src, PI3K./Aktl/eNOS, and ERKs [J]. Am J Physiol Cell Physiol, 2008,295(6) :1647 -1657.
  • 5Vlassara H, Palace M. IL Diabetes and advanced glycation endproducts [J]. Journal of Internal Medicine,2002,251:87 - 101.
  • 6Bierhaus A, Cheviou S, Cheviou M, et al. Advanced glycation end product - induced activation of NF - kB is suppressed byα- lipoic acid in cultured endothelial cells [ J ]. Diabetes, 1997, 46:1481 - 1490.
  • 7Watanabe D, Suzuma K, Suzuma I, et al. Vitreous levels of angiopoietin 2 and vascular endothelial growth factor in patients with proliferative diabetic retinopathy [ J ]. Am J Ophthalmol, 2005,139 (3) : 476 -481.
  • 8Petrovic MG, Korosec P, Kosnik M, et al. Local and genetic determinants of vascular endothelial growth factor expression in advanced proliferative diabetic rotinopathy[ J]. Mol Vis, 2008,30 (14) : 1382 - 1387.
  • 9Arevalo JF, Garcia - Amaris RA. Intravitreal bevaeizumab for diabetic retinopathy[ J ]. Curr Diabetes Rev ,2009,5 (1) :39 -46.
  • 10Yu P, Passam FH, Yu DM ,et al. Beta2 -glycoprotein I inhibits vascular endothelial growth factor and basic fibroblast growth factor - induced angiogencsis through its amino terminal domain [ J]. Journal of Hemostasis & Thrombosis, 2008,6 (7) : 1215 - 1223.

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