SkQR1 Reduces Neurologic Deficit Caused by Rat Brain Compression Ischemia.

Autor: Genrikhs EE; Research Center of Neurology, Moscow, Russia., Stelmashook EV; Research Center of Neurology, Moscow, Russia., Rogozin PD; Research Center of Neurology, Moscow, Russia., Novikova SV; Research Center of Neurology, Moscow, Russia., Aleksandrova OP; Research Center of Neurology, Moscow, Russia., Sobolev VB; Research Center of Neurology, Moscow, Russia., Skrebitsky VG; Research Center of Neurology, Moscow, Russia., Isaev NK; Research Center of Neurology, Moscow, Russia. nisaev61@mail.ru.; M. V. Lomonosov Moscow State University, Moscow, Russia. nisaev61@mail.ru.
Jazyk: angličtina
Zdroj: Bulletin of experimental biology and medicine [Bull Exp Biol Med] 2021 Mar; Vol. 170 (5), pp. 590-593. Date of Electronic Publication: 2021 Mar 31.
DOI: 10.1007/s10517-021-05112-8
Abstrakt: 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.
Databáze: MEDLINE
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