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Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
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Double-edged action of SOD mimetic in diabetic nephropathy

Kensuke Asaba1, Akihiro Tojo, Maristela Lika Onozato

  • 1Division of Nephrology and Endocrinology, University of Tokyo, Tokyo, Japan.

Journal of Cardiovascular Pharmacology
|January 31, 2007
PubMed

Insights

Tempol treatment reduced oxidative stress and glomerular matrix expansion in diabetic nephropathy by suppressing peroxide production. However, it did not decrease hypochlorite or urinary protein excretion.

Area of Science:

  • Nephrology
  • Oxidative Stress Research
  • Pharmacology

Background:

  • Diabetic nephropathy is a significant complication of diabetes mellitus.
  • Oxidative stress is implicated in the pathogenesis of diabetic nephropathy.
  • Superoxide dismutase (SOD) mimetics are potential therapeutic agents.

Purpose of the Study:

  • To investigate the effect of the SOD mimetic, tempol, on diabetic nephropathy.
  • To evaluate the impact of tempol on oxidative stress markers and kidney damage in diabetic rats.

Main Methods:

  • Streptozotocin-induced diabetic rats were treated with tempol for 6 weeks.
  • Evaluated NADPH oxidase expression, catalase and myeloperoxidase (MPO) activity, SOD activity, and production of peroxide and hypochlorite.
  • Assessed transforming growth factor-beta (TGF-beta) and mesangial matrix expansion.

Main Results:

  • Tempol prevented increased NADPH oxidase and peroxide production in diabetic rat glomeruli.
  • Tempol stimulated SOD activity and increased hydrogen peroxide conversion, with enhanced MPO converting it to hypochlorite.
  • Tempol reduced TGF-beta and mesangial matrix expansion but did not reduce hypochlorite or urinary protein excretion.

Conclusions:

  • Tempol inhibited glomerular matrix expansion by suppressing peroxide production and TGF-beta.
  • Tempol failed to reduce proteinuria in diabetic nephropathy, potentially due to increased hypochlorite production.

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