Department of Neurosurgery, Southwest Hospital, Third Military Medical University (Army Medical University), 29 Gaotanyan Street, Shapingba District, Chongqing 400038, China.
Oxid Med Cell Longev. 2020 Jan 4;2020:8285065. doi: 10.1155/2020/8285065. eCollection 2020.
White matter injury (WMI) is an important cause of high disability after intracerebral haemorrhage (ICH). It is widely accepted that reactive oxygen species (ROS) contributes to WMI, but there is still no evidence-based treatment. Here, mitoquinone (MitoQ), a newly developed selective mitochondrial ROS scavenger, was used to test its neuroprotective potential. The data showed that MitoQ attenuated motor function deficits and motor-evoked potential (MEP) latency prolongation. Further research found that MitoQ blunted the loss of oligodendrocytes and oligodendrocyte precursor cells, therefore reduced demyelination and axon swelling after ICH. In the in vitro experiments, MitoQ, but not the nonselective antioxidant, almost completely attenuated the iron-induced membrane potential decrease and cell death. Mechanistically, MitoQ blocked the ATP deletion and mitochondrial ROS overproduction. The present study demonstrates that the selective mitochondrial ROS scavenger MitoQ may improve the efficacy of antioxidant treatment of ICH by white matter injury alleviation.
脑内出血（ICH）后，其致残的重要原因是白质损伤（WMI）。目前广泛认为活性氧（ROS）会导致 WMI，但仍缺乏基于循证的治疗方法。本研究中，一种新型的选择性线粒体 ROS 清除剂米托醌（MitoQ），被用于测试其神经保护作用。数据表明，MitoQ 可减轻运动功能障碍和运动诱发电位（MEP）潜伏期延长。进一步的研究发现，MitoQ 减轻了少突胶质细胞和少突胶质前体细胞的丢失，从而减少了 ICH 后的脱髓鞘和轴突肿胀。在体外实验中，MitoQ 而非非选择性抗氧化剂几乎完全减轻了铁诱导的膜电位降低和细胞死亡。从机制上看，MitoQ 阻断了 ATP 缺失和线粒体 ROS 的过度产生。本研究表明，选择性线粒体 ROS 清除剂 MitoQ 可能通过减轻 WMI 改善 ICH 的抗氧化治疗效果。
