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γ-Glutamylcysteine Alleviates Ischemic Stroke-Induced Neuronal Apoptosis by Inhibiting ROS-Mediated Endoplasmic

Hui-Qin Li1, Sheng-Nan Xia1, Si-Yi Xu1

  • 1Department of Neurology, Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Institute of Brain Science, Nanjing University, Nanjing 210008, China.

Oxidative Medicine and Cellular Longevity
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Summary

Gamma-glutamylcysteine (γ-GC) protects brain cells from oxidative stress and apoptosis during ischemic stroke. This study shows γ-GC may be a promising therapeutic for stroke by reducing reactive oxygen species and endoplasmic reticulum stress.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Ischemic stroke causes significant neuronal damage due to oxidative stress and apoptosis.
  • Reduced glutathione (GSH) levels exacerbate ischemia/reperfusion injury.
  • Targeting oxidative stress and neuronal apoptosis is crucial for stroke recovery.

Purpose of the Study:

  • To investigate the neuroprotective effects of γ-glutamylcysteine (γ-GC), a GSH precursor, against neuronal apoptosis and brain injury in ischemic stroke.
  • To elucidate the underlying mechanisms of γ-GC's action, focusing on oxidative stress and endoplasmic reticulum (ER) stress pathways.

Main Methods:

  • Utilized middle cerebral artery occlusion (MCAO) and oxygen-glucose deprivation/reoxygenation (OGD/R) models in mice and neuronal cell cultures.
  • Assessed oxidative stress markers, including reactive oxygen species (ROS) and GSH levels.
  • Employed transcriptomics and validation studies to identify key molecular pathways affected by γ-GC.

Main Results:

  • Exogenous γ-GC administration significantly mitigated oxidative stress by upregulating GSH and decreasing ROS levels.
  • γ-GC treatment attenuated neuronal apoptosis and reduced brain injury in both in vivo and in vitro models of ischemic stroke.
  • γ-GC inhibited the activation of PERK and IRE1α in the ER stress pathway, thereby reducing penumbra neuronal apoptosis.

Conclusions:

  • γ-GC demonstrates significant neuroprotective effects in models of ischemic stroke.
  • The study identifies the suppression of ROS-mediated ER stress as a key mechanism for γ-GC's therapeutic action.
  • γ-GC holds promise as a novel therapeutic agent for treating ischemic stroke.