首页> 美国卫生研究院文献>Experimental and Therapeutic Medicine >Sevoflurane exerts improved protective effects than propofol on hypoxia-reoxygenation injury by regulating the microRNA-221-5p/ADAM8 axis in cardiomyocytes
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Sevoflurane exerts improved protective effects than propofol on hypoxia-reoxygenation injury by regulating the microRNA-221-5p/ADAM8 axis in cardiomyocytes

机译:通过在心肌细胞中调节MicroRNA-221-5P / ADAM8轴七氟醚施加改善的保护作用。通过在心肌细胞中调节MicroRNA-221-5P / Adam8轴来提高缺氧雷诺损伤

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摘要

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.
机译:心肌缺血再灌注(I / R)损伤是心脏病和死亡的主要原因。降低I / R对临床实践的不利影响仍然是一个紧急问题。本研究检测了麻醉剂(七氟醚和异丙酚),ADAM8和MICRRNA(MIR)-221-5P在缺氧雷诺(H / R)模型中的心肌组织保护中的相互作用。培养H9C2细胞并进行H / R刺激以进一步验证体外。进行逆转录定量PCR或蛋白质印迹以评估mRNA或蛋白质表达水平。细胞计数试剂盒-8,BrdU的,和caspase-3的活性测定法以研究细胞活力,增殖和细胞凋亡。进行双荧光素酶报告器测定以验证miR-221-5p和Adam8之间的关联。通过促进细胞活力,增殖和抑制细胞凋亡,七氟脲对H / R损伤的寿命对H / R损伤的寿命具有更大的保护作用。同时,与异丙酚处理的H / R受损的心肌细胞相比,七氟醚处理的H / R受损心肌细胞的ADAM8的表达水平较高。此外,ADAM8的过度表达促进了H / R损伤的七氟醚处理的心肌细胞的细胞活力和增殖,但抑制细胞凋亡,而MIR-221-5P的下调表现出与ADAM8过表达的相反趋势。本数据提供了证据表明,七氟醚可以介导MIR-221-5P / ADAM8轴,与H / R损伤的心肌细胞中的异丙酚相比,发挥更好的保护作用。

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