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Retigabine attenuates focal cerebral ischemic injury through inhibiting mitochondria-dependent apoptotic pathway

G-B Li1, J-Y Liu, X-M Feng

  • 1Department of Pathology, Changchun Medical College, Changchun, China. zrensheng@sina.com.

European Review for Medical and Pharmacological Sciences
|August 3, 2018
PubMed
Abstract

Insights

Retigabine (RTG) protects against stroke by reducing oxidative stress and cell death. This neuroprotective effect is mediated by inhibiting key inflammatory signaling pathways, offering a potential therapeutic strategy for ischemic injury.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Focal cerebral ischemic injury, often caused by middle cerebral artery occlusion (MCAO), leads to significant neuronal damage.
  • Oxidative stress and apoptosis are key pathological mechanisms in ischemic stroke.
  • Identifying neuroprotective agents is crucial for stroke treatment.

Purpose of the Study:

  • To investigate the neuroprotective effects of retigabine (RTG) on focal cerebral ischemic injury.
  • To elucidate the underlying molecular mechanisms of RTG's protective action.

Main Methods:

  • A mouse model of MCAO was used to induce ischemic injury.
  • Biochemical markers of oxidative stress (MDA, SOD, GSH) were measured.
  • Brain infarct volume, apoptosis (TUNEL), and protein expression (Bcl-2, Bax, caspase 3, p38, JNK) were assessed.

Main Results:

  • RTG treatment significantly reduced brain infarct volume and neurological deficits.
  • RTG decreased malondialdehyde (MDA) levels and increased superoxide dismutase (SOD) and reduced glutathione (GSH) activity.
  • RTG inhibited apoptosis by reducing the Bax/Bcl-2 ratio and cleaved caspase 3 expression, and decreased p38 and JNK phosphorylation.

Conclusions:

  • Retigabine (RTG) demonstrates significant neuroprotective effects against focal cerebral ischemic injury.
  • RTG attenuates ischemic injury by mitigating oxidative stress and inhibiting mitochondria-mediated apoptosis.
  • The mechanism involves the suppression of p38 and JNK phosphorylation pathways.

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