Department of Anesthesiology, The First Hospital Affiliated to Jinzhou Medical University , Jinzhou, P.R. China.
Cell Cycle. 2021 Feb;20(4):383-391. doi: 10.1080/15384101.2021.1875668. Epub 2021 Jan 21.
This project aimed to investigate the protective mechanism of sufentanil pretreatment on myocardial ischemia-reperfusion injury (IRI). An rat model of myocardial IRI and an cultured cardiomyocyte model of hypoxia-reoxygenation (H/R) were used to confirm the anti-oxidation and anti-autophagy effects of sufentanil. The interaction between miR-125a and damage-regulated autophagy regulator 2 (DRAM2) was verified by luciferase reporter assay. We showed that pretreatment with sufentanil suppressed myocardial damage caused by IRI in rats by inhibiting oxidative stress and mitochondrial autophagy. Furthermore, the cardioprotective mechanism of sufentanil was mediated by miR-125a. MiR-125a targeted DRAM2 to ameliorate cardiomyocyte autophagy and oxidative injury following H/R treatment. In conclusion, our results demonstrated that sufentanil pretreatment produced a protective effect against myocardial IRI via regulating miR-125a/DRAM2 signaling axis.
本项目旨在探究舒芬太尼预处理对心肌缺血再灌注损伤（IRI）的保护机制。采用大鼠心肌 IRI 模型和体外培养的心肌细胞缺氧复氧（H/R）模型，证实舒芬太尼的抗氧化和抗自噬作用。通过荧光素酶报告实验验证 miR-125a 与损伤调节自噬调节剂 2（DRAM2）之间的相互作用。结果表明，舒芬太尼预处理通过抑制氧化应激和线粒体自噬抑制大鼠 IRI 引起的心肌损伤。此外，舒芬太尼的心脏保护机制是通过 miR-125a 介导的。miR-125a 通过靶向 DRAM2 减轻 H/R 处理后心肌细胞的自噬和氧化损伤。综上所述，本研究结果表明，舒芬太尼预处理通过调节 miR-125a/DRAM2 信号通路对心肌 IRI 产生保护作用。
