Sevoflurane exerts improved protective effects than propofol on hypoxia‑reoxygenation injury by regulating the microRNA‑221‑5p/ADAM8 axis in cardiomyocytes

Xie,Dan; Deng,Huifei; Feng,Hao

doi:10.3892/etm.2021.10325

Sevoflurane exerts improved protective effects than propofol on hypoxia‑reoxygenation injury by regulating the microRNA‑221‑5p/ADAM8 axis in cardiomyocytes

Authors:
- Dan Xie
- Huifei Deng
- Hao Feng
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Affiliations: Department of Anesthesiology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P.R. China, Department of Neurosurgery, Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College, Nanchong, Sichuan 637000, P.R. China
Published online on: June 18, 2021 https://doi.org/10.3892/etm.2021.10325
Article Number: 893
Copyright: © Xie et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Myocardial ischemia‑reperfusion (I/R) injury is a leading cause of heart disease and death. Decreasing the detrimental effect of I/R remains an urgent issue in clinical practice. The present study examined the interaction of the anesthetics (sevoflurane and propofol), ADAM8, and microRNA (miR)‑221‑5p in myocardial tissue protection in the hypoxia‑reoxygenation (H/R) model. H9C2 cells were cultured and subjected to H/R stimulation for further verifications in vitro. Reverse transcription‑quantitative PCR or western blotting was performed to evaluate mRNA or protein expression levels. Cell Counting Kit‑8, BrdU, and caspase‑3 activity assays were performed to investigate cell viability, proliferation and apoptosis. A dual‑luciferase reporter assay was performed to verify the association between miR‑221‑5p and ADAM8. Sevoflurane had greater protective effects on the life of cardiomyocytes with H/R injury compared with propofol by promoting cell viability, proliferation and inhibiting apoptosis. Concurrently, compared with propofol‑treated H/R injured cardiomyocytes, the expression level of ADAM8 in sevoflurane‑treated H/R injured cardiomyocytes was higher. In addition, overexpression of ADAM8 promoted the cell viability and proliferation of sevoflurane‑treated cardiomyocytes with H/R injury but inhibited cell apoptosis, while the downregulation of miR‑221‑5p showed an opposite trend to that of ADAM8 overexpression. The present data provide evidence that sevoflurane can mediate the miR‑221‑5p/ADAM8 axis, playing a better protective role compared with propofol in cardiomyocytes with H/R injury.

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