The single intravenous administration of mitochondria-targeted antioxidant SkQR1 after traumatic brain injury attenuate neurological deficit in rats.

The single intravenous administration of mitochondria-targeted antioxidant SkQR1 after traumatic brain injury attenuate neurological deficit in rats. Brain Res Bull. 2019 Mar 29;: Authors: Genrikhs EE, Stelmashook EV, Alexandrova OP, Novikova SV, Voronkov DN, Glibka YA, Skulachev VP, Isaev NK Abstract 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 plastoqu...
Source: Brain Research Bulletin - Category: Neurology Authors: Tags: Brain Res Bull Source Type: research

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