Administration of hydrogen sulfide protects ischemia-reperfusion induced acute kidney injury by reducing the oxidative stress

Administration of hydrogen sulfide protects ischemia-reperfusion induced acute kidney injury by reducing the oxidative stress


Authors:

Fatemeh Azizi1, Behjat Seifi1,Mehri Kadkhodaee1 1-Department of Physiology, Medical School, Tehran University of Medical Sciences, Tehran, Iran.

Correspondence:

azizifateme14@yahoo.com

Background: Renal ischemia–reperfusion injury (IRI) is a major cause of acute kidney injury (AKI) [1]. Hydrogen sulfide (H2S) has been known as a novel gaseous signaling molecule [2, 3]. The aim of this study was to investigate whether the efficacy of H2S in protecting against renal IRI is throughits antioxidant effect.

Method:In this study, rats were randomized into Sham, IR, or sodium hydrosulfide (NaHS, an H2S donor) groups. To establish a model of renal IRI, both renal arteries were occluded for 55 min and then declamped to allow reperfusion for 24 hours. Rats in the NaHS group received intraperitoneal injections of 75 μmol/kg NaHS 10 min before the onset of ischemia and immediately after the onset of reperfusion. Sham group underwent laparotomy without cross-clamping of renal pedicles. After reperfusion, plasma and renal tissue samples were collected for functional, histological and oxidative stress evaluation.

Results: The IR group exhibited significant rise in plasma creatinine, BUN,renal MDA concentration and significant reduction of renal SOD activity. Treatment with NaHS reduced the levels of plasma creatinine, BUN, renal MDA concentration and increased SOD activity in the kidneys. NaHS improved renal histological changes in comparison to IR group.

Conclusion: Our data demonstrated that H2S can protect against renal IRI and that its therapeutic effects may be mediated by reducing oxidative stress.