The effects of S-nitrosoglutathione on intestinal ischemia reperfusion injury and acute lung injury in rats: Roles of oxidative stress and NF-κB
Inci Turan, Hale Sayan Ozacmak, VH Ozacmak, F Barut, ID Ozacmak
article (Uluslararası, Hakemli) | Yazar(lar): Inci Turan, Hale Sayan Ozacmak, VH Ozacmak, F Barut, ID Ozacmak | Yıl: 2018 | Dergi/Kurum: TISSUE & CELL | İndeks: WOS.SCI | DOI: 10.1016/j.tice.2018.03.012 | Anahtar Kelimeler: Intestinal ischemia, Reperfusion injury, Lung injury, GSNO — Özet: Background: Intestinal ischem
Background: Intestinal ischemia and reperfusion (I/R) induces oxidative stress, inflammatory response, and acute lung injury. S-nitrosoglutathione (GSNO), a nitric oxide donor, has been documented to have protective effects on experimental ischemia models.
Aim: The aim of this study was to examine the effect of GSNO on I/R-induced intestine and lung damage and detect the potential mechanisms emphasizing the protective role of GSNO.
Methods: Intestinal I/R was induced by occluding the superior mesenteric artery for 30 min followed by reperfusion for 180 min. GSNO was administered intravenously before reperfusion period (0.25 mg/kg). The levels of lipid peroxidation, reduced glutathione, and myeloperoxidase (MPO), histopathological evaluation and immunohistochemical expressions of both nuclear factor KappaB (NF-kappa B) and inducible nitric oxide (iNOS) in intestine and lung tissues were assessed.
Results: Histolopathologic evaluation demonstrated that intestinal I/R induced severe damages in the intestine and the lung tissues. Histopathological scores decreased with GSNO treatment. GSNO treatment reduced lipid peroxidation and MPO levels and inhibited expression of NF-kappa B and iNOS in the intestine.
Conclusion: Our results suggest that GSNO treatment may ameliorate the intestinal and lung injury in rats, at least in part, by inhibiting inflammatory response and oxidative stress.