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Simvastatin attenuates contrast-induced nephropathy through modulation of oxidative stress, proinflammatory

Ketab E Al-Otaibi1, Abdulrahman M Al Elaiwi, Mohammad Tariq

  • 1Department of Urology, Prince Sultan Medical Military City, Riyadh, Saudi Arabia.

Oxidative Medicine and Cellular Longevity
|October 26, 2012
PubMed

Insights

Simvastatin (SSTN) protects against contrast media-induced nephropathy by reducing oxidative stress and inflammation. This study demonstrates SSTN

Area of Science:

  • Nephrology
  • Pharmacology
  • Toxicology

Background:

  • Contrast media-induced nephropathy (CMN) is a significant clinical challenge.
  • Pathophysiology of CMN is not fully understood, limiting prophylaxis strategies.

Purpose of the Study:

  • Investigate the roles of oxidative stress, myeloperoxidase (MPO), and nitric oxide in iohexol-induced nephropathy.
  • Evaluate the nephroprotective effects of simvastatin (SSTN) in this model.

Main Methods:

  • Adult Sprague Dawley rats underwent water deprivation and glycerol injection to induce kidney injury.
  • Iohexol was administered intravenously, followed by daily oral administration of simvastatin (15, 30, 60 mg/kg) for 4 days.
  • Kidney function (creatinine, urea) and histological changes were assessed; oxidative stress markers (lipid hydroperoxides, glutathione) and MPO activity were measured.

Main Results:

  • Simvastatin dose-dependently attenuated increases in creatinine and urea, and reduced structural kidney damage.
  • SSTN reversed CM-induced increases in oxidative stress and MPO activity, and normalized nitric oxide levels.
  • These findings indicate a significant nephroprotective effect of simvastatin.

Conclusions:

  • Oxidative stress, MPO, and altered nitric oxide signaling contribute to contrast media-induced nephropathy.
  • Simvastatin demonstrates significant nephroprotective potential against CMN.
  • SSTN may be a viable therapeutic strategy for preventing contrast media-induced kidney injury.

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