Osthole ameliorates renal ischemia-reperfusion injury by inhibiting inflammatory response

Urol Int. 2013;91(3):350-6. doi: 10.1159/000347191. Epub 2013 Mar 23.

Abstract

Introduction: Renal ischemia-reperfusion (I/R) injury is a primary cause of acute renal failure that results in high mortality. This study aimed to investigate the effect of osthole, a natural coumarin derivative, on renal I/R injury in a rat model.

Materials and methods: Rats were randomly allocated to the sham operation + vehicle, I/R + vehicle, and I/R + osthole groups. Renal I/R injury was induced by clamping the left renal artery for 45 min followed by 12 h of reperfusion and a contralateral nephrectomy. Osthole (40 mg/kg) was intraperitoneally injected 30 min before inducing I/R. Renal function and histological damage were determined subsequently. Myeloperoxidase activity, monocyte/macrophage infiltration, as well as tumor necrosis factor-α, IL-1β, and activated p38 mitogen-activated protein kinase expression in kidneys were also assessed.

Results: Osthole treatment significantly ameliorated I/R-induced renal functional and morphological injuries. Moreover, osthole treatment attenuated myeloperoxidase activity, monocyte/macrophage infiltration, and tumor necrosis factor-α, IL-1β, and activated p38 mitogen-activated protein kinase expression in kidneys.

Conclusions: Osthole treatment ameliorates renal I/R injury by inhibiting inflammatory responses in kidneys. Thus, osthole may represent a novel practical strategy to prevent renal I/R injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Kidney Injury / prevention & control
  • Animals
  • Calcium Channel Blockers / therapeutic use*
  • Coumarins / therapeutic use*
  • Disease Models, Animal
  • Gene Expression Regulation, Enzymologic
  • Inflammation / prevention & control*
  • Interleukin-1beta / metabolism
  • Kidney / drug effects*
  • Kidney / enzymology
  • Male
  • Monocytes / cytology
  • Peroxidase / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / therapy*
  • Tumor Necrosis Factor-alpha / metabolism
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Calcium Channel Blockers
  • Coumarins
  • Interleukin-1beta
  • Tumor Necrosis Factor-alpha
  • Peroxidase
  • p38 Mitogen-Activated Protein Kinases
  • osthol