miR‑320‑3p is involved in morphine pre‑conditioning to protect rat cardiomyocytes from ischemia/reperfusion injury through targeting Akt3
Affiliations: Department of Anesthesiology, Tiantai People's Hospital of Zhejiang Province, Tiantai, Zhejiang 317200, P.R. China, Department of Orthopedics, Tiantai People's Hospital of Zhejiang Province, Tiantai, Zhejiang 317200, P.R. China
- Published online on: May 27, 2020 https://doi.org/10.3892/mmr.2020.11190
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Morphine pre‑conditioning (MPC) can significantly reduce myocardial ischemic injury and inhibit cardiomyocyte apoptosis, but the underlying mechanism still remains unclear. The aim of the present study was to investigate the protective mechanism of MPC in myocardial hypoxia/reoxygenation (H/R) injury at the microRNA (miR) level. H9c2 cells were used as a model of H/R and subjected to morphine pre‑treatment. The protective effects of MPC on H/R injury in cardiomyocytes were evaluated using MTT and colorimetric assay, as well as flow cytometry. In addition, reverse transcription‑quantitative PCR, western blotting and dual‑luciferase reporter assay experiments were performed to determine the relationship between MPC, miR‑320‑3p and Akt3, and their effects on H/R injury. The present study demonstrated that MPC enhanced cell activity, decreased LDH content, and reduced apoptosis in rat cardiomyocytes, suggesting that MPC could protect these cells from H/R injury. Moreover, MPC partially reversed the increase in miR‑320‑3p expression and the decrease in Akt3 levels caused by H/R injury. Inhibition of miR‑320‑3p expression also attenuated the effects of H/R on cardiomyocyte activity, LDH content and apoptosis. Furthermore, Akt3 was predicted to be a target gene of miR‑320‑3p, and overexpression of miR‑320‑3p inhibited the expression of Akt3, blocking the protective effects of MPC on the cells. The current findings revealed that MPC could protect cardiomyocytes from H/R damage through targeting miR‑320‑3p to regulate the PI3K/Akt3 signaling pathway.