The protective effects of prostaglandin E1 on lung injury following renal ischemia-reperfusion in rats.


Oztay F., Kara-Kisla B., Orhan N., Yanardag R., Bolkent Ş.

Toxicology and industrial health, cilt.32, ss.1684-92, 2016 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 32
  • Basım Tarihi: 2016
  • Doi Numarası: 10.1177/0748233715576615
  • Dergi Adı: Toxicology and industrial health
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.1684-92
  • Anahtar Kelimeler: Renal ischemia-reperfusion, lung injury, PGE1, oxidative stress, edema, rat, ISCHEMIA/REPERFUSION INJURY, FAILURE, PATHOPHYSIOLOGY, CROSSTALK, PRODUCTS, BLOOD, LEADS, E(1)
  • İstanbul Üniversitesi Adresli: Evet

Özet

For the purposes of the present study, the protective effect of prostaglandin E1 (PGE1) on lung injury following renal ischemia-reperfusion (RIR) was investigated. Adult male rats were divided into four groups, namely, (I) control rats given physiological saline; (II) rats given PGE1 (20 mu g/kg, intravenously); (III) rats subjected to RIR; and (IV) rats subjected to RIR given PGE1 30 min prior to ischemia and just before reperfusion. The right nephrectomy was performed in the RIR model. The left renal pedicle was occluded for 60 min to induce ischemia and then the left kidney was subjected to reperfusion for 60 min. The lungs of rats were used for microscopic and biochemical analyses. Although rats subjected to RIR did not exhibit heavy degenerative alterations in the lung structure, they possessed pulmonary interstitial edema. Lung glutathione levels and catalase, superoxide dismutase, glutathione peroxidase, and tissue factor (TF) activities were decreased in rats subjected to RIR, while lung lipid peroxidation, myeloperoxidase (MPO), xanthine oxidase and serum lactate dehydrogenase (LDH) activities, and blood urea and serum creatinine levels were increased in these rats when compared with the control group. PGE1 treatments resulted in the regression of oxidative stress via induction of antioxidant system, the decreased MPO and LDH activities, the reduced urea and creatinine levels, and the induced TF activity in rats subjected to RIR, while edema still remained permanent. We conclude that PGE1 may be useful in preventing lung injury with the exception of edema that occurred as a result of RIR in rats.