PMID: 30018728Jul 19, 2018Paper

Mitochondrial-targeted antioxidant MitoQ provides neuroprotection and reduces neuronal apoptosis in experimental traumatic brain injury possibly via the Nrf2-ARE pathway

American Journal of Translational Research
Jian ZhouMengliang Zhou

Abstract

Mitoquinone (MitoQ) is a powerful mitochondrial-targeted antioxidant whose neuroprotective effects have been shown in a variety of animal models of neurological diseases. However, its roles in traumatic brain injury (TBI) remain unexplored. The primary objective of this study was to investigate the neuroprotection afforded by MitoQ in a mouse model of TBI, and the involvement of the Nrf2-ARE signaling pathway in the putative neuroprotective mechanism. Mice were randomly divided into four groups: sham group, TBI group, TBI + vehicle group, and TBI + MitoQ group. MitoQ (4 mg/kg, administered intraperitoneally) or an equal volume of vehicle was given at 30 min after TBI. After 24 h, brain samples were harvested for analysis. The results demonstrated that treatment with MitoQ significantly improved neurological deficits, alleviated brain edema and inhibited cortical neuronal apoptosis. Furthermore, MitoQ administration increased the activity of antioxidant enzymes, including superoxide dismutase (SOD) and glutathione peroxidase (GPx), whereas it decreased the malondialdehyde (MDA) content. In addition, MitoQ treatment reduced Bax protein translocation to mitochondria and cytochrome c release into the cytosol. Moreover, MitoQ greatl...Continue Reading

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