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Original Research Article | OPEN ACCESS

Protective effect of dexmedetomidine pre-treatment against myocardial ischemia-reperfusion injury in rats

Qin Sha, Hui Jiang

Department of Anesthesiology, Qingpu Branch of Zhongshan Hospital, Fudan University, Shanghai 201700, China;

For correspondence:-  Hui Jiang   Email: shasha222_1983@163.com

Accepted: 30 January 2023        Published: 28 February 2023

Citation: Sha Q, Jiang H. Protective effect of dexmedetomidine pre-treatment against myocardial ischemia-reperfusion injury in rats. Trop J Pharm Res 2023; 22(2):349-354 doi: 10.4314/tjpr.v22i2.18

© 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 determine the protective effect of dexmedetomidine pre-treatment against myocardial ischemia-reperfusion injury (MRI), and the involvement of ER stress and protein kinase R-like ER enzyme (PERK) signaling pathway in the process.
Methods: Sixty male Sprague-Dawley (SD) rats were assigned to three groups: sham, model (ischemia-reperfusion), and dexmedetomidine pre-treatment groups. Myocardial infarction area was measured using 2,3,5-triphenyl tetrazolium chloride (TTC) method. Changes in heart structure were examined using H & E, while myocardial cell apoptosis was determined with TUNEL assay. The protein expression levels of CHOP, glucose regulatory protein 78, ATF4, eukaryotic translation initiation factor 2-α (elf2-α), and PERK were assayed with Western blotting.
Results: RPP, myocardial infarction area, myocardial cell apoptosis rate, and the expression levels of CHOP, GRP78, ATF4, elf2-α, and PERK were significantly raised, relative to sham. The structure of myocardial cells in sham-operated rats was intact and orderly. In contrast, the arrangement of myocardial cells in the model group was disordered, and the myofibrils were broken or wavy. However, the arrangement of myocardial cells in the dexmedetomidine group was significantly improved, when compared with the model group.
Conclusion: Pretreatment with dexmedetomidine may exert a protective effect against MRI through suppression of ER stress and PERK signaling pathway. Further preclinical studies would be required to validate these findings.

Keywords: Dexmedetomidine, ER stress, PERK signaling pathway, Ischemia-reperfusion injury, Myocardial protection

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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