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Original Research Article | OPEN ACCESS

Dexmedetomidine mitigates myocardial ischemia-reperfusion injury via regulation of HMGB1-TLR4-NF-κB signaling axis

Ting Wen1, Jia Liu2, Shibiao Chen1, Benchao Hou1, Gan Li1, Chaxiu Yu1

1Department of Anesthesiology, The First Affiliated Hospital of Nanchang University, Jiangxi Province, China; 2Department of Laboratory, Jiangxi Provincial Mental Hospital, Nanchang 330006, Jiangxi Province, China.

For correspondence:-  Chaxiu Yu   Email: pj295h@163.com

Accepted: 22 October 2021        Published: 30 November 2021

Citation: Wen T, Liu J, Chen S, Hou B, Li G, Yu C. Dexmedetomidine mitigates myocardial ischemia-reperfusion injury via regulation of HMGB1-TLR4-NF-κB signaling axis. Trop J Pharm Res 2021; 20(11):2273-2278 doi: 10.4314/tjpr.v20i11.6

© 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..

Abstract

Purpose: To study the effect of dexmedetomidine (Dex) on myocardial ischemia-reperfusion injury (MIRI), and the associated mechanism of action.
Methods: Sixty Sprague-Dawley (SD) rats were assigned to sham, ischemia-reperfusion (I/R), Dex, and MD groups (methyllycaconitine prior to injection with Dex), with 15 rats in each group. Pathological changes in myocardial tissues were determined in all groups. Protein expression levels of HMGB1, TLR4, NF-κB and myeloid differentiation protein 88 (MyD88) in serum and myocardial tissues were assayed and compared.
Results: Protein levels of HMGB1, TLR4, MyD88 and NF-κB were significantly higher in heart muscle I/R rats than those in sham group, but lower in heart muscle of rats in Dex group than in heart muscle of I/R rats (p < 0.05). However, they were significantly up-regulated in MD group, relative to Dex group (p < 0.05).
Conclusion: Dex exerts a protective effect against ischemia/reperfusion-induced myocardial damage via HMGB1-TLR4-NF-κB signal axis via CAP, and thus, is a potential agent for the management of myocardial disease.

Keywords: Ischemia/reperfusion injury, Dexmedetomidine, activation of high mobility group box 1, HMGB1, Toll-like receptor 4, Myocardial ischemia reperfusion in

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

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