Ulinastatin suppresses systemic inflammatory response following lung ischemia-reperfusion injury in rats

Transplant Proc. 2008 Jun;40(5):1310-1. doi: 10.1016/j.transproceed.2008.01.082.

Abstract

Objective: We sought to investigate whether ulinastatin (urinary trypsin inhibitor) inhibited systemic inflammatory responses following lung ischemia-reperfusion (I/R) injury.

Materials and methods: Establishing a steady left lung warm I/R model in rats, we randomly divided 32 animals into 4 groups: sham (n = 8); I/R (n = 8); low-dose ulinastatin (5000 U/kg pre-ischemia) + I/R (n = 8); and high-dose ulinastatin (10,000 U/kg pre-ischemia) + I/R (n = 8). Measured variables included plasma concentrations of tumor necrosis factor-alpha (TNF-alpha), as well as interleukin (IL)-6 and IL-8.

Results: The serum concentrations of TNF-alpha, IL-6, and IL-8 in the ulinastatin pretreated groups were markedly decreased compared with those of the I/R group (P < .05). The levels of TNF-alpha, IL-6, and IL-8 were lower in the high-dose ulinastatin group compared with the low-dose ulinastatin group (P < .05).

Conclusion: Ulinastatin produced dose-dependent attenuation of the systemic inflammatory response of rats following lung I/R injury.

MeSH terms

  • Animals
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Glycoproteins / blood
  • Glycoproteins / therapeutic use*
  • Inflammation / etiology
  • Inflammation / prevention & control*
  • Male
  • Pulmonary Circulation / drug effects
  • Pulmonary Circulation / physiology*
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / complications
  • Reperfusion Injury / drug therapy*
  • Thoracotomy
  • Trypsin Inhibitors / blood
  • Trypsin Inhibitors / therapeutic use*

Substances

  • Glycoproteins
  • Trypsin Inhibitors
  • urinastatin