The proinflammatory cytokine-mediated protective effects of pentoxifylline, iloprost, and cilostazol on a mitigating lung injury induced by lower limb ischemia and reperfusion in rats

Hidiroǧlu M., UĞUZ E., Özerdem G., Yildiz E., Berkan ö.

Turkish Journal of Thoracic and Cardiovascular Surgery, vol.22, no.1, pp.138-144, 2014 (SCI-Expanded) identifier

  • Publication Type: Article / Article
  • Volume: 22 Issue: 1
  • Publication Date: 2014
  • Doi Number: 10.5606/tgkdc.dergisi.2014.8304
  • Journal Name: Turkish Journal of Thoracic and Cardiovascular Surgery
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, TR DİZİN (ULAKBİM)
  • Page Numbers: pp.138-144
  • Keywords: Cilostazol, Iloprost, Ischemia-reperfusion injury, Lung injury, Pentoxifylline
  • Ankara Yıldırım Beyazıt University Affiliated: Yes


Background: This study aims to elucidate whether pentoxifylline, iloprost and cilostazol mitigates acute lung injury induced by lower limb ischemia-reperfusion (I/R) and their protective effects cover cytokines. Methods: Forty rats were randomized into five groups: control (group 1), ischemia-reperfusion (group 2), pentoxifylline (group 3), iloprost (group 4), iloprost and cilostazol (group 5). All drugs were administered before ischemia. Samples were obtained for tumor necrosis factoralpha (TNF-a), interleukin 6 (IL-6), and total sialic acid (TSA) assays. Findings of lung injury were examined. Results: Interleukin-6 and TNF levels were increased at 90 minutes and sustained elevated even after 240 minutes. In groups 3 and 4, IL-6 and TNF levels were significantly lower at 90, 180 and 240 minutes compared to group 2. At 180 minutes, TSA levels in groups 2, 3, 4 and 5 were significantly different from baseline and 90 minute levels. At this time point, TSA levels of group 2 and 3 were significantly higher compared to group 4 and 5. Conclusion: In this acute lung injury model induced by I/R of the lower limbs, pretreatment with pentoxifylline, iloprost and cilostazol significantly attenuated proinflammatory activities and parenchymal lung damage.