Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Dexmedetomidine pre-conditioning induces inhibition of ROS in myocardial ischemia-reperfusion injury in rats through AMPK pathway

Shanhu Wu, Wanping Hong, Xue'e Su, Jinwei Liang

Department of Anaesthesiology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, Fujian Province, China;

For correspondence:- Jinwei Liang Email: kouzhuang99035134@163.com

Accepted: 26 July 2023 Published: 31 August 2023

Citation: Wu S, Hong W, Su X, Liang J. Dexmedetomidine pre-conditioning induces inhibition of ROS in myocardial ischemia-reperfusion injury in rats through AMPK pathway. Trop J Pharm Res 2023; 22(8):1605-1611 doi: 10.4314/tjpr.v22i8.11

© 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 elucidate the basis for the cardioprotective effect of dexmedetomidine pre-treatment on ROS-induced myocardial ischemia-reperfusion injury (IRI) in rats.

Methods: Sixty Sprague-Dawley (SD) rats were assigned to sham, model and dexmedetomidine intervention groups, each having 20 rats. Myocardial IRI was induced in the model and dexmedetomidine intervention groups using modified suture method. In sham group, chests of rats were opened, but without ligation, while dexmedetomidine intervention group was pre-treated with dexmedetomidine (5 μg/kg) before establishment of the IRI model. Protein expressions of adenosine 5‘-monophosphate (AMP)-activated protein kinase (AMPK) was determined by Western blot assay. Mean fluorescence intensity of ROS was measured using flow cytometry.

Results: AMPK protein was significantly down-regulated in model rats, relative to sham rats, but significantly higher in dexmedetomidine intervention rats (p < 0.05). In model rats, mean ROS fluorescence intensity and degree of apoptosis of cardiomyocytes were higher than the corresponding values in sham rats (p < 0.05), but lower in dexmedetomidine intervention group.

Conclusion: Dexmedetomidine reduces oxidative stress in myocardial tissue and exerts a protective role by activating AMPK pathway and inhibiting mitochondrial generation of ROS. Therefore, this compound might have a potential clinical role in the management of IRI.

Keywords: Dexmedetomidine premedication, Adenylate-activated protein kinase, Reactive oxygen species, Myocardial ischemia-reperfusion injury, Myocardial protect