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西地那非对糖尿病大鼠肾脏的保护作用及机制

Protective effects of sildenafil on the kidney of diabetic rats and the mechanism
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摘要 目的探讨西地那非对糖尿病大鼠肾脏的保护作用及机制。方法将28只雄性SD大鼠分为正常对照组、正常+西地那非处理组、糖尿病组、两地那非治疗组,每组7照。药物十预8周后,检测各组大鼠的血糖(BG)、24h尿白蛋白量、肌酐水平。随后处死大鼠.测定肾组织中总抗氧化能力(T—AOC)、丙二醛(MDA)含量、谷胱甘肽过氧化酶(GSHPX)活性。同时留取肾组织作HE染色行病理检查。RTPCR法检测肾组织中单核细胞趋化蛋白-1(MCP-1)mRNA表达。结果与糖尿病组相比,西地那非治疗组BG无统计学差异,而24h尿内蛋白量、Ccr、MDA、MCP1mRNA表达牡著下降,T-AOC、GSHPX活性上升,差异具有统计学意义,肾组织病理改变减轻。结论西地那非可以改善糖尿病大鼠肾脏损害,其机制可能与其抗氧化、降低MCP-1表达有关。 Objective To investigate the protective effects of sildenafii oil the kidney of diabetic rats and the mechanism. Methods 28 male SD rats were equally divided into four groups: normal rats,normal rats treated with sildenafil, diabetic rats, diabetic rats treated with sildenafil. After 8 weeks, blood glucose, blood creatinine and 24 h urinary albumin were measured. 1.ipid peroxidatin, ma londialdehye(MDA), glutathione peroxidase (GSH-PX) and total antioxidative capacity (T-AOC) in the renal tissues were determined. The renal tissue was cxamined by light microscopy. The expression levels of monocyte chemoattractant protein I (MCP-1) mRNA were semi-quantitatively detected by reverse transcription-polymerase chain reaction. Results No significant differences in blood glucose were found between diabetic group and sildenafil treated groups. As compared with diabetic group, the levels of Ccr,24-h urinary albumin, renal MDA, MCP 1 mRNA were decreased significantly, but the activity of renal GSH PX and T-AOC increased significantly in sildenafil-treated groups. Renal pathologic changes in sildenafil-treated group were also alleviated. Conclusion Sildenafil could alleviate the renal pathologic changes in diabetic rats, which is closely related to the antioxidization and the decrease of MCP-1 activity in renal tissue.
出处 《临床肾脏病杂志》 2009年第12期558-561,F0003,共5页 Journal Of Clinical Nephrology
关键词 大鼠 糖尿病肾病 氧化性应激 丙二醛 Rats Diabetic kidney diseases Oxidative stress Malondialdehyde
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  • 1Hemnes AR, Zaiman A, Champion HC. PDE5A inhibition attenuates bleo-mycin-induced pulmonary fibrosis and pulmonary hypertension through inhibition of ROS generation and RhoA/Rho kinase activation. Am J Physiol Lung Cell Mol Physiol, 2008, 1 : 24-33.
  • 2Fernandes MA, Marques RJ, Vicente JA, et al. Sildenafil citrate concentrations not affecting oxidative phosphorylation depress H2O2 generation by rat heart mitochondria. Mol Cell Biochem, 2008,309:77- 85.
  • 3Tan Air, Forbes JM, Cooper ME. AGE, RAGE and ROS in diabetic nephropathy. Semin Nephrol, 2007,27 : 130-143.
  • 4Vasavada N, Agarwal R. Role of oxidative stress in diabetic nephropathy. Adv Chronic Kidney Dis, 2005,12 : 146- 154.
  • 5Camera A, Hopps E,Caimi G. Diabetic microangiopathy: Physiopathological, clinical and therapeutic aspects. Minerva Endocrinol, 2007,32 : 209- 229.
  • 6包艳,贾汝汉,袁军,李竞,叶迎春,孙永林,王颖.罗格列酮对糖尿病大鼠肾脏保护作用机制的探讨[J].中华肾脏病杂志,2007,23(4):224-229. 被引量:18
  • 7陈玲,贾汝汉,丁国华,刘红燕,杨定平,彭隽,田少江.缬草油对2型糖尿病大鼠肾脏的保护作用及其机制探讨[J].中华肾脏病杂志,2003,19(3):168-172. 被引量:42
  • 8Chen L,Jia RH, Qiu CJ, ct al. Hyperglycemia inhibits the uptake of dehydroascorbate in tubular epithelial cell. Am J Nephrol,2005,5 : 459-465.
  • 9Lee HB, Yu MR, Yang Y, et al. Reactive oxygen species regulated signaling pathways in diabetic nephropathy. J Am Soc Nephrol, 2003,14:241 -245.
  • 10Bao Y,Jia RH, Yuan J, et al. Rosiglitazone ameliorates diabetic nephropathy by inhibiting reactive oxygen species and its down- stream signaling pathways. Pharmacology, 2007,80 : 57-64.

二级参考文献40

  • 1陈磊,秦路平,郑汉臣.缬草的化学成分、植物资源和药理活性[J].药学实践杂志,2000,18(5):277-279. 被引量:15
  • 2包艳,贾汝汉,袁军,李竞,叶迎春,孙永林,王颖.罗格列酮对糖尿病大鼠肾脏保护作用机制的探讨[J].中华肾脏病杂志,2007,23(4):224-229. 被引量:18
  • 3Brownlee M. The pathobiology of diabetic complications: a unifying mechanism. Diabetes, 2005, 54: 1615-1625.
  • 4Villegas I, Martin AR, Toma W, et al. Rosiglitazone, an agonist of peroxisome proliferator-activated receptor gamma, protects against gastric ischemia-reperfusion damage in rats: role of oxygen free radicals generation. Eur J Pharmacol, 2004, 505: 195-203.
  • 5Collino M, Aragno M, Mastrocola R, et al. Modulation of the oxidative stress and inflammatory response by PPAR- gamma agonists in the hippocampus of rats exposed to cerebral ischemia/reperfusion. Eur J Pharmacol, 2006, 530: 70-80.
  • 6Kwan J, Wang H, Munk S, et al. In high glucose protein kinase C-zeta activation is required for mesangial cell generation of reactive oxygen species. Kidney Int, 2005, 68: 2526-2541.
  • 7Lee HB, Yu MR, Yang Y, et al. Reactive oxygen speciesregulated signaling pathways in diabetic nephropathy. J Am Soc Nephrol, 2003, 14(8 Suppl 3): S241-S245.
  • 8Wada T, Yokoyama H, Matsushima K, et al. Monocyte chemoattractant protein-1: does it play a role in diabetic nephropathy? Nephrol Dial Transplant, 2003, 18: 457-459.
  • 9Ha H, Yu MR, Choi YJ, et al. Role of high glucoseinduced nuclear factor-kappaB activation in monocyte chemoattractant protein-1 expression by mesangial cells. J Am Soc Nephrol, 2002, 13: 894-902.
  • 10Ha H, Lee HB. Reactive oxygen species as glucose signaling molecules in mesangial cells cultured under high glucose. Kidney Int Suppl, 2000, 77: S19-$25.

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