Platonin mitigates acute lung injury induced by bilateral lower limb ischemia-reperfusion in rats

J Surg Res. 2011 May 15;167(2):e255-62. doi: 10.1016/j.jss.2010.03.075. Epub 2010 Apr 24.

Abstract

Background: Oxidative stress and inflammatory response are crucial in mediating the development of acute lung injury induced by bilateral lower limb ischemia-reperfusion (I/R). Platonin, a potent antioxidant, possesses anti-inflammation capacity. We sought to elucidate whether platonin could mitigate acute lung injury induced by lower limb I/R.

Materials and methods: Forty-eight adult male rats were allocated to receive I/R, I/R plus platonin (100 μg/kg intravenous injection immediately after reperfusion), sham instrumentation, or sham instrumentation plus platonin (denoted as the I/R, I/R-platonin, Sham, or Sham-platonin group, respectively; n = 12 in each group). Bilateral hind limb I/R was induced by applying rubber band tourniquets high around each thigh for 3 h followed by reperfusion for 3 h. After sacrifice, the degree of lung injury was determined.

Results: Histologic findings revealed moderate inflammation in lung tissues of the I/R group and mild inflammation in those of the I/R-platonin group. Total cell number and protein concentration in bronchoalveolar lavage fluid as well as the leukocyte infiltration and myeloperoxidase activity in lung tissues of the I/R group were significantly higher than those of the I/R-platonin group. The pulmonary concentrations of macrophage inflammatory protein-2, interleukin-6, and prostaglandin E(2) of the I/R group were significantly higher than those of the I/R-platonin group. Moreover, the plasma nitric oxide concentration as well as the nitric oxide and malondialdehyde concentrations in lung tissues of the I/R group were significantly higher than those of the I/R-platonin group.

Conclusions: Platonin mitigates acute lung injury induced by bilateral lower limb I/R in rats.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Lung Injury / etiology*
  • Acute Lung Injury / metabolism
  • Acute Lung Injury / prevention & control*
  • Animals
  • Antioxidants / administration & dosage
  • Antioxidants / pharmacology
  • Antioxidants / therapeutic use*
  • Chemokine CXCL2 / metabolism
  • Dinoprostone / metabolism
  • Injections, Intravenous
  • Interleukin-6 / metabolism
  • Leukocytes / pathology
  • Lower Extremity / blood supply*
  • Male
  • Malondialdehyde / metabolism
  • Models, Animal
  • Nitric Oxide / metabolism
  • Oxidative Stress / drug effects
  • Oxidative Stress / physiology
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / complications*
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / physiopathology
  • Thiazoles / administration & dosage
  • Thiazoles / pharmacology
  • Thiazoles / therapeutic use*

Substances

  • Antioxidants
  • Chemokine CXCL2
  • Cxcl2 protein, rat
  • Interleukin-6
  • Thiazoles
  • platonin
  • Nitric Oxide
  • Malondialdehyde
  • Dinoprostone