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SkQR1 Reduces Neurologic Deficit Caused by Rat Brain Compression Ischemia.

E E Genrikhs1, E V Stelmashook1, P D Rogozin1

  • 1Research Center of Neurology, Moscow, Russia.

Bulletin of Experimental Biology and Medicine
|March 31, 2021
PubMed
Summary

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Antioxidant SkQR1 demonstrated neuroprotective effects in a rat model of stroke, significantly reducing neurological deficits after ischemic injury. However, SkQR1 did not improve recovery in an in vitro model of hippocampal slices.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Ischemic Stroke Research

Background:

  • Ischemic stroke poses a significant health challenge, leading to neuronal damage and functional deficits.
  • Antioxidants are being investigated for their potential to mitigate stroke-induced injury.
  • The antioxidant SkQR1's efficacy in stroke models requires further elucidation.

Purpose of the Study:

  • To evaluate the neuroprotective potential of the antioxidant SkQR1 in a rat model of focal cerebral ischemia.
  • To assess the impact of SkQR1 on neurological deficits and motor function following ischemic injury.
  • To investigate SkQR1's effect on neuronal recovery in an in vitro model of ischemia using hippocampal slices.

Main Methods:

  • A left-sided compression ischemia model was induced in rats to simulate stroke.
Keywords:
acute hippocampal slicescompression ischemiamitochondrial-targeted antioxidantsneuronspopulation excitatory postsynaptic potentials (pEPSP)

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  • Neurological deficits and forelimb motor function were assessed post-ischemia.
  • SkQR1 was administered intravenously 30 minutes after the ischemic event.
  • An in vitro model using rat hippocampal slices was employed to study ischemia and reperfusion effects.

    • Main Results:

    • A 2.5-minute ischemia caused no significant functional deficits in rats.
    • Increased compression time led to dose-dependent neurological deficits.
    • A single intravenous injection of SkQR1 (250 nmol/kg) significantly reduced neurological deficits.
    • In vitro, 15-minute ischemia inhibited hippocampal excitatory postsynaptic potentials, with no recovery during reperfusion.
    • Preincubation with SkQR1 did not significantly improve potential recovery in the in vitro model.

    Conclusions:

    • The antioxidant SkQR1 exhibits significant neuroprotective effects in an in vivo rat model of focal cerebral ischemia.
    • SkQR1 administration effectively reduces neurological deficits following ischemic injury.
    • SkQR1's therapeutic benefit may be context-dependent, as it did not enhance recovery in the in vitro hippocampal slice model.