Yan Jing,
Li Yao,
Weicui Du,
Jia Liu,
Rongrong Yang,
Wanchang Zhou,
Xiaolin Xu,
Jingjing Cao,
Lichao Zhang,
Chengjing Si 
For correspondence:- Chengjing Si Email: kpcpu5@163.com
Accepted: 28 June 2021 Published: 29 July 2021
Citation: Jing Y, Yao L, Du W, Liu J, Yang R, Zhou W, et al. Dexmedetomidine inhibits oxidative stress in sepsis-induced acute kidney injury in rats by regulating GSK-3 β/Nrf2/ARE axis. Trop J Pharm Res 2021; 20(7):1381-1386 doi: 10.4314/tjpr.v20i7.9
© 2021 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..
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 of 10 mg/kg, dexmedetomidine (Dex) group, and glycogen synthase kinase-3 beta (GSK-3β) inhibitor group given sb216763. In addition, Dex and inhibitor groups received the same dose of lipopolysaccharide as model group. There were 10 rats in each group. Pathological changes in kidney tissue, and the levels of related oxidative stress indices were determined.
Results: Compared with the model group, granular degeneration of renal tubular epithelial cells was significantly reduced in Dex group, and the population of exfoliated cells decreased (p < 0.05). The levels of malondialdehyde (MDA) and reactive oxygen species (ROS) in dexmedetomidine and GSK-3β inhibitor groups were significantly reduced, while superoxide dismutase (SOD), glutathione (GSH) and catalase (CAT) activities were markedly raised, relative to model group (p < 0.05). Protein levels of p-GSK-3β and Nrf2 markedly were raised in dexmedetomidine and GSK-3β inhibitor groups (p < 0.01). After intervention with Dex and GSK-3β inhibitor, there were marked upregulations in mRNA and protein ex
Conclusion: Dexmedetomidine ameliorates SAKI injury in rats via suppression of oxidative stress. Its mechanism of action may be related to the regulation of GSK-3β/Nrf2/ARE signaling pathway. This finding may be a novel approach to the clinical management of SAKI.
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