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

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)-221-5...

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Bibliographic Details
Published in:Experimental and therapeutic medicine 2021-08, Vol.22 (2), Article 893
Main Authors: Xie, Dan, Deng, Huifei, Feng, Hao
Format: Article
Language:English
Subjects:
Anesthesia
Antibodies
Apoptosis
Biotechnology
Cardiomyocytes
Care and treatment
Cell growth
Comparative analysis
Gene expression
Genetic aspects
Health aspects
Heart attacks
Heart cells
Hypoxia
MicroRNA
MicroRNAs
Myocardial ischemia
Propofol
Proteases
Proteins
Reperfusion injury
Sevoflurane
Testing
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Summary: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.
ISSN:1792-0981
1792-1015
DOI:10.3892/etm.2021.10325