Department of Anesthesiology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.
Department of Anesthesiology, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Biomed Res Int. 2017;2017:1314297. doi: 10.1155/2017/1314297. Epub 2017 Jun 6.
In several recent studies, proteomics analyses suggest that increase of ubiquinol-cytochrome c reductase core protein 1 (UQCRC1) is cardio-protective. However, direct evidence for this effect has not yet been obtained. Thus, the current study aimed to determine this effect and the mechanism underlying this effect. The results showed that overexpression of UQCRC1 protected H9c2 cardiac cells against in vitro simulated ischemia-reperfusion by maintaining mitochondrial membrane potential and suppressing the expression of caspase-3. These protective effects were significantly enhanced by exogenous Zn but completely abolished by Zn-selective chelator TPEN. Furthermore, the upregulation of UQCRC1 reduced the concentration of free Zn in mitochondria, whereas the downregulation of UQCRC1 increased the concentration of free Zn in mitochondria. In conclusion, the overexpression of UQCRC1 can protect H9c2 cardiac cells against simulated ischemia/reperfusion, and this cardio-protective effect is likely mediated by zinc binding.
在最近的几项研究中，蛋白质组学分析表明，泛醌-细胞色素 c 还原酶核心蛋白 1（UQCRC1）的增加具有心脏保护作用。然而，尚未获得这一效应的直接证据。因此，本研究旨在确定这种效应及其潜在机制。结果表明，过表达 UQCRC1 通过维持线粒体膜电位和抑制半胱天冬酶-3 的表达，保护 H9c2 心肌细胞免受体外模拟缺血再灌注损伤。外源性 Zn 显著增强了这些保护作用，而 Zn 选择性螯合剂 TPEN 则完全消除了这些作用。此外，UQCRC1 的上调降低了线粒体中游离 Zn 的浓度，而下调 UQCRC1 的表达则增加了线粒体中游离 Zn 的浓度。总之，UQCRC1 的过表达可以保护 H9c2 心肌细胞免受模拟缺血/再灌注损伤，这种心脏保护作用可能是通过锌结合介导的。
