a The First Affiliated Hospital of Xi'an Jiaotong University , Xi'an , P. R. China.
b The Productive Medicine Center, Tangdu Hospital , Air Force Military Medical University , Xi'an , P. R. China.
Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):1248-1255. doi: 10.1080/21691401.2019.1594243.
Mitochondrial dysfunction is a major contributory factor for myocardial ischemia-reperfusion (I/R) injury. It has been reported that Pink1-Parkin-mediated mitochondrial autophagy could effectively remove damaged mitochondria and excess ROS to ensure the stability of intracellular mitochondria. The present study was designed to evaluate whether the polymerized porcine haemoglobin (pPolyHb), a novel type of haemoglobin oxygen carrier, has an effect on I/R injury via regulating the Pink1-Parkin mediated mitochondrial autophagy pathway in myocardial H9C2 cells. The results revealed that pPolyHb could effectively reduce apoptosis and improve the survival rates of H9C2 cells. In addition, Pink1 and Parkin levels gradually decreased with pPolyHb reoxygenation. The inhibition of mitochondrial autophagy through mitochondrial-division inhibitor-1(mdivi-1) resulted in a decrease in anti-apoptotic protein Bcl-2 and an increase in pro-apoptotic protein Bax and CytC. In conclusion, pPolyHb has a protective effect on myocardial ischemia-reperfusion injury by regulating moderate mitochondrial autophagy.
线粒体功能障碍是心肌缺血再灌注（I/R）损伤的主要因素之一。有报道称，Pink1-Parkin 介导的线粒体自噬可以有效清除受损线粒体和过量的 ROS，从而确保细胞内线粒体的稳定性。本研究旨在评估新型血红蛋白氧载体聚合猪血红蛋白（pPolyHb）是否通过调节心肌 H9C2 细胞中的 Pink1-Parkin 介导的线粒体自噬途径对 I/R 损伤产生影响。结果表明，pPolyHb 可有效减少细胞凋亡，提高 H9C2 细胞的存活率。此外，随着 pPolyHb 复氧，Pink1 和 Parkin 的水平逐渐降低。通过线粒体分裂抑制剂-1（mdivi-1）抑制线粒体自噬会导致抗凋亡蛋白 Bcl-2 减少，促凋亡蛋白 Bax 和 CytC 增加。总之，pPolyHb 通过调节适度的线粒体自噬对心肌缺血再灌注损伤具有保护作用。
