Zhihai Geng1,
Xuelian Zhu1,
Xi Han2,
Xianfeng Xin1 
For correspondence:- Xianfeng Xin Email: ct44cn@163.com
Accepted: 26 February 2020 Published: 31 March 2020
Citation: Geng Z, Zhu X, Han X, Xin X. Effect of dexmedetomidine post-treatment on oxidative stress and apoptosis induced by myocardial ischemia-reperfusion injury in rats. Trop J Pharm Res 2020; 19(3):571-575 doi: 10.4314/tjpr.v19i3.16
© 2020 The authors.
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Purpose: To study the effect of dexmedetomidine on myocardial ischemia-reperfusion injury (MI/RI)-induced imbalance on oxidant-prooxidant status and apoptotic changes in rats.
Methods: Ninety (90) male Wistar rats were randomly divided into three groups – sham, model and post-treatment. In model rats, the anterior descending branch of the left coronary artery was ligated for 25 min, prior to their being subjected to reperfusion for 2 h. Rats in the post-treatment group were subjected to ligation at the anterior descending branch of the left coronary artery for 25 min, but they were intravenously injected with dexmedetomidine at a dose of 10 μg/kg prior to reperfusion. There was no ligation in the sham group. Malondialdehyde (MDA), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were assayed. Lactate dehydrogenase (LDH) and creatine kinase isoenzyme (CK-MB) levels were also evaluated. Apoptosis was measured with TdT-mediated dUTP nick end labeling (TUNEL) assay.
Results: Compared with the sham group, MDA level in the model group was significantly rose, while SOD and GSH-Px activities were markedly decreased (p < 0.05). Moreover, there were higher LDH and CK-MB activities in model rats than in the sham rats, but they were significantly lower in the post-treatment group than in the model group (p < 0.05). Apoptosis was higher in model rats than in sham operation rats, but was markedly decreased in post-treatment rats than in model rats (p < 0.05).
Conclusion: Post-treatment with dexmedetomidine exerts myocardial protective effect via significant reduction in oxidative stress-induced myocardial injury and apoptosis.
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