SkQR1 Reduces Neurologic Deficit Caused by Rat Brain Compression Ischemia

The protective effect of antioxidant SkQR1 was examined on the model of left-sided compression ischemia in rat sensorimotor cortex. The special tests aimed to determine the neurologic deficit in the limbs and assess performance of the forelimbs showed that a 2.5-min ischemia produced no disturbance...

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Bibliographic Details
Published in:Bulletin of experimental biology and medicine 2021-03, Vol.170 (5), p.590-593
Main Authors: Genrikhs, E. E., Stelmashook, E. V., Rogozin, P. D., Novikova, S. V., Aleksandrova, O. P., Sobolev, V. B., Skrebitsky, V. G., Isaev, N. K.
Format: Article
Language:English
Subjects:
Animals
Antioxidants
Antioxidants - therapeutic use
Biomedical and Life Sciences
Biomedicine
Body weight
Brain
Brain Ischemia - drug therapy
Brain Ischemia - metabolism
Brain slice preparation
Cell Biology
Compression
Cortex (somatosensory)
Excitatory postsynaptic potentials
Excitatory Postsynaptic Potentials - drug effects
General Pathology and Pathological Physiology
Hippocampus
Hippocampus - drug effects
Hippocampus - metabolism
Internal Medicine
Intravenous administration
Ischemia
Laboratory Medicine
Male
Methylene blue
Mitochondria - drug effects
Mitochondria - metabolism
Neuroprotective Agents - therapeutic use
Pathology
Plastoquinone - analogs & derivatives
Plastoquinone - therapeutic use
Rats
Reperfusion
Rhodamines - therapeutic use
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Summary:The protective effect of antioxidant SkQR1 was examined on the model of left-sided compression ischemia in rat sensorimotor cortex. The special tests aimed to determine the neurologic deficit in the limbs and assess performance of the forelimbs showed that a 2.5-min ischemia produced no disturbance in the limb functions on postsurgery days 1, 3, and 7. Elevation of compression time resulted in neurologic deficit in animals, and its severity depended on this time. A single intravenous injection of SkQR1 (250 nmol/kg body weight) performed 30 min after ischemia significantly reduced the degree of neurologic deficit. In vitro model of ischemia in surviving rat hippocampal slices showed that a 15-min-long ischemia significantly inhibited the population excitatory postsynaptic potentials, which did not restore during reperfusion. Preincubation of the slices with SkQR1 did not significantly affect recovery of these potentials.
ISSN:0007-4888
1573-8221
DOI:10.1007/s10517-021-05112-8