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抗氧化剂对糖尿病大鼠肾小球蛋白激酶C的影响 被引量:1

Effect of Antioxidants on Reduction of PKC in Diabetic Rats
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摘要 目的 通过大鼠糖尿病模型 ,观察抗氧化剂对糖尿病大鼠肾小球蛋白激酶的影响。方法 将 75只雄性Wistar大鼠分为正常对照组、糖尿病未治疗组、抗氧化剂治疗组各 2 5只 ,共观察 8周 ,分别测定尿白蛋白排泄量(UAE) ,内生肌酣消除率 (Ccr)、血浆及肾脏组织一氧化氮 (NO)、一氧化氮合成酶 (NOS)、内皮素 (ET)和肾小球蛋白激酶C(proteinkinaseC ,PKC)。结果 给予维生素E治疗组 8周时 ,Ccr[(5 .2 8± 0 .5 4)ml/(min·kg) ]及尿白蛋白排泄量 [(14.2 7± 1.16 ) μg/2 4h]显著低于未治疗组 ,肾小球细胞膜PKC[(6 8.2 7± 12 .33) pmol/(min·mgprotein) ],2周时N0 [(34 .2 3± 3.91) μmol/L]及NOS[(32 .0 7± 3.76 )U/L]明显低于未治疗组 ,维生素E治疗组 2周时与 8周时的NO及NOS下降幅度明显小于未治疗组。结论 维生素E具有抑制PKC活性作用。 Objective To investigate the effect of vitamin E on reduction of PKC activity in streptozotocine induced diabetic rats.Methods Vitamin E 20 mg/kg/d was given to diabetic rats for 8 weeks. Urinary albumin excretion (UAE) was measured by radioimmunoassay. The changes of creatinine clearence rate (Ccr), nitric oxide (NO), nitric oxide synthase (NOS) and endothelin (ET) in plasma and renal cortical tissue, membrane protein kinase C (PKC) in renal glomeruli were observed.Results After the treatment of vitamin C, Ccr (4.61±0.12 ml/min/kg), UAE (17.40±1.22 μg/24 h), PKC (60.21±9.78 pmol/min/mg protein) at 8th week decreased significantly. Both NO(30.23±2.01 μmol/L) and NOS (35.21±1.54 U/L) in plasma and kidney tissue were lowered as compared with untreated diabetic group in second week. Vitamin E also delayed in lowering NO and NOS levels in 8 weeks.Conclusion Vitamin E can reduce PKC activity in diabetic rats.
出处 《同济大学学报(医学版)》 CAS 2002年第2期90-92,共3页 Journal of Tongji University(Medical Science)
基金 铁道部医学专项基金资助项目 (TW 2 0 0 2 30 )
关键词 抗氧化剂 糖尿病肾病 蛋白激酶C 大鼠 antioxidant diabetic nephropathy protein kinase C rats
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  • 1[1]Park SH, Choi HJ, Lee JH, et al. High glucose inhibits renal proximal tubule cell proliferation and involves PKC,oxidative stress, and TGF- beta 1 [J]. Kidney Int, 2001,59(5): 1695 - 705.
  • 2[2]Cha DR,Kim NH, Yoon JW, et al. Role of vascular endothelial growth factor in diabetic nephropathy[J ]. 2000,58 (Suppl 77) :104 - 112.
  • 3[3]Park SH,Choi HJ,Lee JH, et al. High glucose stimulates Ca2 + uptake via cAMP and PLC/PKC pathways in primary cultured renal proximal tubule cells [ J ]. Kidney Blood Press Res,2001,24(1) :10- 17.
  • 4[4]Chen S, Cohen MP, Lautenslager GT, et al. Glycated albumin stimulates TGF-beta1 production and protein kinase C activity in glomerular endothelial cells[J ]. Kidney Int,2001,59(2) :673 - 681.
  • 5[5]Mene P, Festuccia F. Diabetic nephropathy and advanced glycation end products [J]. Contrib Nephrol, 2001,131(2) :22 - 32.

同被引文献7

  • 1Axelsson J. Obesity in chronic kidney disease: good or bad?[J]. Blood Purif, 2008,26(1) : 23 -29.
  • 2Ramos LF, Shimani A, Lkizler TA, et al. Oxidative Stress and Inflammation Are Associated with Adiposity in Moderate to Severe CKD [J ]. J Am Soc Nephrol, 2008,19 : 593 - 599.
  • 3Khan NI, Naz L, Yasrneen G. Obesity: an independent risk factor for systemic oxidative stress [ J ]. Pak J Pharm Sci, 2006,19 : 62 - 65.
  • 4Basu S. Isoprostanes: novel bioactive products of lipid peroxidation [J].Free Radic Res, 2004, 38 ( 2 ) : 105 - 122.
  • 5Witko-Sarsat V, Friedlander M, Capeillere-Blandin C, et al. Advanced oxidation protein products as a novel marker of oxidative stress in uremia [ J ]. Kidney Int, 1996,49(5) : 1304 - 1313.
  • 6Drueke T, Witko-Sarsat V, Massy ZA, et al. Iron Therapy, advanced oxidation protein products and carotid artery intima media thickness in end stage renal disease [J].Circulation, 2002,106 ( 17 ) : 2212 - 2217.
  • 7Witko-Sarsat V, Friedlander M, Nguyen-Khoa T, et al. Advanced oxidation protein products as novel mediators of inflammation and monocyte activation in chronic renal failure [ J ]. J Immunol, 1998, 161 : 2524 - 2532.

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