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.
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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