ubiquinone and Cerebral-Hemorrhage

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.

Topics: Animals; Cerebral Hemorrhage; Mice; Mitochondria; Organophosphorus Compounds; Reactive Oxygen Species; Ubiquinone; White Matter

Topics: Animals; Anti-Inflammatory Agents; Brain; Brain Edema; Cell Line; Cerebral Hemorrhage; Cytokines; Disease Models, Animal; Inflammasomes; Mice, Inbred C57BL; Microglia; Mitochondria; NLR Family, Pyrin Domain-Containing 3 Protein; Organophosphorus Compounds; Phenotype; Reactive Oxygen Species; Signal Transduction; Ubiquinone