The renoprotective effect of cGMP phosphodiesterase inhibitor and nitroprusside in a rat model of cyclosporin A-induced nephrotoxicity

Clin Nephrol. 2013 Jul;80(1):53-62. doi: 10.5414/CN107571.

Abstract

Background: The cyclosporin A (CsA) nephrotoxicity limits its usefulness as an immunosuppression. We studied the administration of both nitroprusside and phosphodiesterase-5 inhibitor (udenafil) in order to determine whether these agents could ameliorate the renal injury in CsA nephrotoxicity.

Methods: 30 8-week-old SD rats were divided into 5 groups: the control (1), SQ with 15 mg/kg CsA (Group 2), CsA along with 5 mg/kg IP nitroprusside (Group 3), CsA with 10 mg/kg PO udenafil (Group 4), and CsA with udenafil and nitroprusside (Group 5).

Results: Group showed an increase in creatinine compared o the control group. Group 5 showed a decrease in creatinine compared to Group 2. In TUNEL, Group 2 increased apoptosis in proximal tubules compared to control. Group 5 showed a decrease in apoptosis compared to Groups 2, 3, and 4. In IHC, the eNOS in Group 2 was stronger than in the controls. Groups 3, 4, and 5 showed decreased staining intensity compared to Group 2. In IHC, the VEGF in Groups 2, 3, and 4 increased compared to the controls. The eNOS protein expression was increased in both Groups 3 and 5 compared to the controls. The VEGF protein expression was increased in Groups 3 and 5 compared to Group 2. The eNOS mRNA was decreased in Group 2 compared to the control group and tended to increase in Groups 3, 4, and 5 compared to Group 2. The VEGF mRNA was increased in Group 2 and tended to increase more in Groups 3 and 5.

Conclusion: The udenafil and nitroprusside ameliorated renal injury in rat model of CsA nephrotoxicity. The mechanism appears to be associated with decreasing tubular apoptosis by decreasing eNOS and increasing VEGF.

MeSH terms

  • Acute Kidney Injury / chemically induced
  • Acute Kidney Injury / metabolism*
  • Acute Kidney Injury / prevention & control*
  • Analysis of Variance
  • Animals
  • Apoptosis / drug effects
  • Blood Urea Nitrogen
  • Creatinine / blood
  • Cyclosporine / adverse effects
  • Disease Models, Animal
  • Kidney Tubules, Proximal / drug effects
  • Kidney Tubules, Proximal / pathology
  • Male
  • Nitric Oxide Donors / therapeutic use*
  • Nitric Oxide Synthase Type III / genetics
  • Nitric Oxide Synthase Type III / metabolism
  • Nitroprusside / therapeutic use*
  • Phosphodiesterase 5 Inhibitors / therapeutic use*
  • Pyrimidines / therapeutic use*
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Statistics, Nonparametric
  • Sulfonamides / therapeutic use*
  • Vascular Endothelial Growth Factor A / genetics
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Nitric Oxide Donors
  • Phosphodiesterase 5 Inhibitors
  • Pyrimidines
  • RNA, Messenger
  • Sulfonamides
  • Vascular Endothelial Growth Factor A
  • Nitroprusside
  • Cyclosporine
  • Creatinine
  • Nitric Oxide Synthase Type III
  • udenafil