The single intravenous administration of mitochondria-targeted antioxidant SkQR1 after traumatic brain injury attenuates neurological deficit in ratsстатья

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Дата последнего поиска статьи во внешних источниках: 11 декабря 2019 г.

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[1] The single intravenous administration of mitochondria-targeted antioxidant skqr1 after traumatic brain injury attenuates neurological deficit in rats / E. E. Genrikhs, E. V. Stelmashook, O. P. Alexandrova et al. // Brain Research Bulletin. — 2019. — Vol. 148. — P. 100–108. The protective effect of SkQR1, a mitochondria-targeted antioxidant, was investigated on the model of focal one-sided traumatic brain injury (TBI) of the sensorimotor cortex region from 1 to 7 days after the injury. TBI caused a reliable disruption of the functions of the limbs contralateral to injury focus. The intravenous single injection of SkQR1 (250 nmol/kg) but not C12R1 (a SkQR1 homologue devoid of the antioxidant group) 30 min after TBI reduced the impairment of the motor functions of the limbs. A statistically significant improvement in limb function in animals was shown using 3 different tests: limb-placing test, beam-walking test and grip strength test. A pronounced therapeutic effect appeared on the 1th day and lasted until the end of the experiment - the 7th day after TBI. Histopathological examination showed that in the group of animals that did not receive SkQR1 in the marginal layer of the lesion there was a marked increase in astroglial expression, infiltration with segmented neutrophils, and poor survivability of neurons compared with animals treated with SkQR1. The obtained results demonstrate that the single use of plastoquinone-containing mitochondria-targeted antioxidant SkQR1 at the early stages of development of traumatic brain damage can reduce TBI-related disruptions of limb functions, and that mechanisms of the brain damage after trauma are dependent on the production of mitochondrial reactive oxygen species. [ DOI ]

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