Dexmedetomidine inhibits oxidative stress in sepsis-induced acute kidney injury in rats by regulating GSK-3β/Nrf2/ARE axis

Purpose: To determine the effect of dexmedetomidine on sepsis-mediated acute kidney injury (SAKI) in rats.
 Methods: Twenty-four SD rats were randomly divided into blank untreated control group, model group given lipopolysaccharide at a dose 10 mg/kg, (Dex) and glycogen synthase kinase-3 beta (GSK-3β) inhibitor sb216763. In addition, Dex groups received same as group. There each Pathological changes tissue, levels related oxidative stress indices determined.
 Results: Compared with granular degeneration renal tubular epithelial cells was significantly reduced population exfoliated decreased (p < 0.05). The malondialdehyde (MDA) reactive oxygen species (ROS) GSK-3β reduced, while superoxide dismutase (SOD), glutathione (GSH) catalase (CAT) activities markedly raised, relative to Protein p- Nrf2 raised 0.01). After intervention inhibitor, there marked upregulations mRNA protein expression heme oxygenase-1 (HO-1), when compared 0.05).
 Conclusion: Dexmedetomidine ameliorates SAKI via suppression stress. Its mechanism action may be regulation GSK-3β/Nrf2/ARE signaling pathway. This finding novel approach clinical management SAKI.