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

BACKGROUND: Renal ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury. Hydrogen sulfide (H2S) has been known as a novel gaseous signaling molecule. AIMS: The aim of this study was to investigate whether the efficacy of H2S in protecting against renal IRI is through its antioxidative 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 h. 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, blood urea nitrogen (BUN), renal malondialdehyde (MDA) concentration, and significant reduction of renal superoxide dismutase (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.

Hepatoprotective effects of remote perconditioning during renal ischemia.

BACKGROUND: Novel treatment strategies are required to reduce the development of hepatic injury during surgical procedure in which renal ischemia/reperfusion (IR) is inevitable. Remote perconditioning (rPeC) has been proved to reduce the extent of kidney damages induced by renal IR injury. The aim of this study was to determine the protective effect of rPeC against hepatic injury caused by renal ischemia. METHODS: Male rats were subjected to the right nephrectomy and randomized as: sham, no additional intervention; IR, 45 min of left renal pedicle occlusion; rPeC, four cycles of 5-min limb IR administered at the beginning of renal ischemia. After 24-h of reperfusion, the plasma and tissue samples were taken. RESULTS: A significant improvement in hepatic functional injury and oxidative damages were observed in the rPeC group compared to the IR group. However, histological evaluation and plasma levels of TNF-α revealed no significant difference among groups. CONCLUSIONS: It is concluded that rPeC exerted protective effects on renal IR-induced hepatic injury as a remote organ. The protection may be a consequence of the reduction in oxidative stress in the liver. This simple approach may be a promising strategy against IR-induced remote organ damages in the clinical practice (Fig. 4, Ref. 23).