Key result
Hydrogen sulfide donor NaHS attenuates acute renal ischemia-reperfusion injury by lowering NF-kB and ICAM-1.
Why the study?
Renal ischemia-reperfusion injury is a major issue in kidney transplant, prompting investigation into whether prophylactic hydrogen sulphide donor treatment could minimize injury in hypertensive rats with acute renal failure.
Does prophylactic treatment with sodium hydrosulfide reduce renal ischemia-reperfusion injury in normotensive and hypertensive rats with acute renal failure?
Does prophylactic treatment with sodium hydrosulfide reduce renal ischemia-reperfusion injury in normotensive and hypertensive rats with acute renal failure?
Prophylactic treatment with a hydrogen sulphide donor attenuates renal ischemia-reperfusion injury and acute renal failure severity in both normotensive and hypertensive rat models.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for H2S donors in renal IRI; human trials required before any clinical consideration.
(Background and Objectives): Renal ischemia perfusion injury is one of the major issues in kidney transplant. The aim of the study was to investigate the hypothesis that prophylactic treatment—with a hydrogen sulphide donor to an acute renal failure case of hypertensive rats—can minimize the ischemia reperfusion injury of the kidney which is beneficial for kidney transplant. To check this hypothesis, the present study was designed to investigate the effect of chronic administration of a hydrogen sulphide (H2S) donor and sodium hydrosulfide (NaHS) on nuclear factor kappa B (NF-kB) and inter cellular adhesion molecule-1 (ICAM-1) concentration in non-renal failure (NRF) and acute renal failure (ARF) rats in the ischemia-reperfusion injury (IRI) model of the kidney in both normotensive WKY and hypertensive rats (L-nitro arginine methyl ester (L-NAME-induced); (Materials and Methods): A total number of 48 Sprague-Dawley rats were recruited into eight groups each consisting of six animals. Each of these eight groups was used to measure systemic and renal parameters, H2S, antioxidant parameters in plasma, plasma concentration of NF-kB and ICAM-1 and renal cortical blood pressure. ARF was induced by single intraperitoneal (i.p.) cisplatin injection (5 mg/kg). Hypertension was induced by oral administration of L-NAME in drinking water for four weeks at 40 mg/kg/day. NaHS was administered (i.p) at 56 µmol/kg for five weeks while dL-propargylglycine (PAG), a H2S generation inhibitor, was administered as a single intra-peritoneal injection (50 mg/kg). An acute surgical experiment was performed for the induction of renal ischemia for 30 min by renal artery clamping followed by reperfusion for three hours; (Results): Chronic administration of NaHS attenuated the severity of ARF in both normotensive and hypertensive animals (L-NAME) along with lowering the blood pressure in hypertensive groups. NaHS improved the oxidative stress parameters such as total superoxide dismutase (T-SOD), glutathione (GSH) and reduced the malondialdehyde (MDA) concentration along with reduction of NF-kB and ICAM-1 following renal IRI; Conclusions: These findings demonstrate that H2S not only reduced the severity of cisplatin induced ARF but also reduced the severity of renal IRI by upregulating antioxidants along with decreased concentrations of NF-kB and ICAM-1 in normotensive and L-NAME induced hypertensive rats.
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Ashfaq Ahmad (2022) studied Acute renal failure and renal ischemia-reperfusion injury (n=48). Sodium hydrosulfide (NaHS, hydrogen sulphide donor) vs. Saline or dL-propargylglycine (PAG) was evaluated on NF-kB and ICAM-1 concentrations (severity of renal ischemia-reperfusion injury) (p=<0.05). Prophylactic treatment with a hydrogen sulphide donor (NaHS) significantly attenuated the severity of acute renal failure and ischemia-reperfusion injury by decreasing NF-kB and ICAM-1 concentrations.
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