Antioxidants
PGC1α/SIRT3-Mediated Oxidative Stress and Downregulation of NLRP3 Expression by Sodium Thiosulfate Pre- and Post-Treatment Accelerates Recovery from Ischemia–Reperfusion-Induced Acute Kidney Injury
By George Johnson Dugbartey, Liam McFarlane, Talal Shamma and 4 others.
Abstract
Background
Renal ischemia–reperfusion injury (IRI) is the leading cause of acute kidney injury (AKI). It is associated with reduced blood flow as encountered in vascular surgery, including aortic aneurysm repair and kidney transplantation. In this study, we investigated whether pre- and/or post-administration of sodium thiosulfate (STS), an FDA-approved hydrogen sulfide donor drug, attenuated IRI-induced AKI in rats.
Methods
AKI was induced in male rats by clamping both renal arteries for 60 min. At 30 min before clamping, and 30 min after reperfusion, STS was administered at a weigh-based dose to achieve a circulating concentration of 150 μM, after which the rats were kept in metabolic cages for urine and blood collection on postoperative days (POD) 3, 5, and 7. Rats were sacrificed on POD3, POD5, and POD7, and kidneys were harvested for analysis. Sham-operated rats received no treatment.