Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Dexmedetomidine preconditioning alleviates apoptosis in rat cardiomyocytes by suppressing programmed cell death 4 (PDCD4) after myocardial ischemia-reperfusion injury

Mengning Wan, Hong Li , Yupei Chen, Guangming Yan, Yue Pi, Youliang Deng

Department of Anesthesiology, The Second Affiliated Hospital of Army Medical University, Chongqing 400037, China;

For correspondence:- Hong Li Email: lihong00611@163.com Tel:+862368774992

Accepted: 26 October 2020 Published: 30 November 2020

Citation: Wan M, Li H, Chen Y, Yan G, Pi Y, Deng Y. Dexmedetomidine preconditioning alleviates apoptosis in rat cardiomyocytes by suppressing programmed cell death 4 (PDCD4) after myocardial ischemia-reperfusion injury. Trop J Pharm Res 2020; 19(11):2309-2315 doi: 10.4314/tjpr.v19i11.9

© 2020 The authors.
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Abstract

Purpose: To determine the role of dexmedetomidine (Dex) in hypoxia/reoxygenation (H/R)-induced myocardial cell injury and the possible involvement of the programmed cell death 4 (Pdcd4) gene in Dex-mediated myocardial cell apoptosis after ischemia-reperfusion (I/R) injury.

Methods: An in vivo I/R-injured rat model and in vitro H/R rat cell model were evaluated to ascertain the role of Dex in apoptosis. Programmed cell death 4 (PDCD4) gene expression levels were measured after Dex preconditioning. The effects of Pdcd4 knockdown or overexpression on Dex-mediated apoptosis during H/R injury were determined.

Results: Dex pretreatment alleviated myocardial infarction in rats, suppressed myocardial cell apoptosis, and inhibited PDCD4 expression (p < 0.05). Treatment with Dex also alleviated H/R-induced apoptosis in rat cardiomyocytes, while PDCD4 expression decreased after Dex treatment (p < 0.05). Moreover, PDCD4 overexpression reversed the inhibitory effect of Dex on H/R myocardial cell apoptosis.

Conclusion: Dex alleviates myocardial infarction in rats via its effect on PDCD4 expression. Therefore, Dex can potentially be used for the treatment but this has to clinical studies.

Keywords: Acute myocardial infarction (AMI), Myocardial ischemia and reperfusion injury (MIRI), Dexmedetomidine (Dex), Programmed cell death 4 (PDCD4), Apoptosi