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 ...
Source: Brain Research Bulletin - Category: Neurology Authors: Tags: Brain Res Bull Source Type: research