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Original Research Article | OPEN ACCESS

Sevoflurane improves renal ischemia-reperfusion injury in rats through RISK signaling pathway

Bo Wang1, Xin Yan2, Xin Zou2

1Department of Anesthesiology, The Third Hospital of Wuhan, Wuhan 430074, China; 2Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

For correspondence:-  Xin Zou   Email: 13972506238@163.com   Tel:+8602784309779

Accepted: 29 July 2023        Published: 31 August 2023

Citation: Wang B, Yan X, Zou X. Sevoflurane improves renal ischemia-reperfusion injury in rats through RISK signaling pathway. Trop J Pharm Res 2023; 22(8):1597-1604 doi: 10.4314/tjpr.v22i8.10

© 2023 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..

Abstract

Purpose: To investigate the effect of sevoflurane on renal ischemia-reperfusion injury (IRI) in rats and its regulatory effect on reperfusion injury salvage kinase (RISK) signaling pathway.
Methods: A total of thirty (30) Sprague-Dawley rats were randomly divided into sham, model and sevoflurane groups with 10 animals per group. Renal IRI models were created in model and sevoflurane groups, while sham group had no ligation. Renal injury was determined using hematoxylin and eosin (HE) staining. Blood urea nitrogen (BUN) and serum creatinine (Scr) levels were assayed while apoptosis was determined via terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining. Enzyme-linked immunosorbent assay (ELISA) was used to assess malonaldehyde (MDA) content and inflammatory factors in kidney tissues and peripheral blood, respectively. Reactive oxygen species (ROS) level was determined using 2,7-dichlorodi-hydro fluorescein diacetate (DCFH-DA) while Western blotting was used to determine the expression of apoptosis- and RISK signaling pathway-related proteins in kidney tissues.
Results: Compared to model group, renal injury in sevoflurane group rats was significantly alleviated (p < 0.01). The levels of BUN and Scr in peripheral blood, apoptosis level in kidney tissues, MDA content and ROS level in kidney tissues, interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α) and IL-6 content, and content of caspase-3 protein in kidney tissues were significantly reduced (p < 0.01), whereas IL-10 content, Bcl-2/Bax ratio and expression levels of p-ERK1/2, p-Akt and phosphorylated glycogen synthase kinase 3β (p-GSK-3β) were significantly increased (p < 0.01) in the sevoflurane group.
Conclusion: Sevoflurane represses the release of inflammatory factors, lowers ROS level and apoptosis of renal cells and improves renal function through activation of RISK signaling pathway in kidney tissues of rats with renal IRI. Thus, sevoflurane is a potential agent for the treatment of IRI.

Keywords: Sevoflurane, Renal IRI, Apoptosis, RISK signaling pathway

Impact Factor
Thompson Reuters (ISI): 0.6 (2023)
H-5 index (Google Scholar): 49 (2023)

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