Research Center of Neurology, Moscow, Russia.
M. V. Lomonosov Moscow State University, Moscow, Russia.
Bull Exp Biol Med. 2021 Mar;170(5):590-593. doi: 10.1007/s10517-021-05112-8. Epub 2021 Mar 31.
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.
抗氧化剂 SkQR1 的保护作用在左侧压迫性缺血大鼠感觉运动皮层模型中进行了研究。专门的测试旨在确定四肢的神经功能缺损，并评估前肢的表现，结果显示 2.5 分钟的缺血在手术后第 1、3 和 7 天不会引起肢体功能障碍。增加压迫时间会导致动物出现神经功能缺损，其严重程度取决于压迫时间。缺血后 30 分钟单次静脉注射 SkQR1（250nmol/kg 体重）可显著降低神经功能缺损的程度。在存活的大鼠海马切片的体外缺血模型中，15 分钟的缺血显著抑制了群体兴奋性突触后电位，在再灌注期间没有恢复。用 SkQR1 对切片进行预孵育不会显著影响这些电位的恢复。
