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Oxycodone protects cardiomyocytes from ischemia-reperfusion-induced apoptosis via PI3K/Akt pathway

Zhao, S.; Zhang, C.; Pi, Z.; Li, R.; Han, P.; Guo, L.

Die Pharmazie 75(9): 430-435

2020


ISSN/ISBN: 0031-7144
PMID: 32797768
Accession: 072267742

Ischemia/reperfusion (I/R) cause secondary myocardial damage following a blood reflow after myocardial infarction. This study aimed to explore oxycodone as a myocardial protector after an I/R injury in rats. Oxycodone reduced myocardial infarction volume, an I/R-induced apoptosis of the cardiomyocytes, the serum levels of CK-MB and LDH. The ejection fraction and fraction shortening in the I/R rats also increased. From the molecular mechanism, it was evident that oxycodone not only decreased the expression levels of Bax, active-caspase 3 protein but also increased the expression levels of Bcl2, p-PI3K, and p-Akt protein in heart tissue of the I/R rats. In vitro, oxycodone induced anti-H9c2 cell apoptosis after hypoxia/reoxygenation (H/R). However, its ability to act as a myocardial protector deteriorated in the presence of a PI3K/Akt pathway inhibitor.

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