Inhibition of Mitochondrial ROS by MitoQ Alleviates White Matter Injury and Improves Outcomes after Intracerebral Haemorrhage in Mice

Weixiang Chen, Chao Guo, Zhengcai Jia, Jie Wang, Min Xia, Chengcheng Li, Mingxi Li, Yi Yin, Xiaoqin Tang, Tunan Chen, Rong Hu, Yujie Chen, Xin Liu, Hua Feng, Pamela M. Martin

Research output: Contribution to journalArticlepeer-review

25 Scopus citations

Abstract

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.

Original languageEnglish (US)
Article number8285065
JournalOxidative medicine and cellular longevity
Volume2020
DOIs
StatePublished - 2020

ASJC Scopus subject areas

  • Biochemistry
  • Aging
  • Cell Biology

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