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

七氟烷通过调节心肌细胞中的 microRNA-221-5p/ADAM8 轴对缺氧-复氧损伤发挥比丙泊酚更好的保护作用

阅读:7
作者:Dan Xie, Huifei Deng, Hao Feng

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.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。