Normobaric oxygen therapy attenuates hyperglycolysis in ischemic stroke

Area of Science:

• Neuroscience
• Biochemistry
• Stroke Research

Background:

• Acute ischemic stroke triggers a pathogenic cascade.
• Normobaric oxygen therapy (NBOT) is a potential neuroprotective strategy.
• Mechanisms of NBOT neuroprotection, particularly cerebral hyperglycolysis, require elucidation.

Purpose of the Study:

• To investigate the role of cerebral hyperglycolysis in NBOT's neuroprotective effects against ischemic stroke.
• To examine the impact of NBOT on key hyperglycolytic enzymes and signaling pathways.

Main Methods:

• Middle cerebral artery occlusion (MCAO) model in Sprague-Dawley rats.
• Administration of 95% oxygen NBOT or room air post-ischemia.
• Assessment of infarct volume, neurological deficits, reactive oxygen species (ROS), and ATP levels.
• Analysis of glucose transporter (GLUT) 1/3, phosphofructokinase 1 (PFK1), lactate dehydrogenase (LDH), and adenosine monophosphate-activated protein kinase (AMPK) expression.

Main Results:

• NBOT significantly reduced infarct volume, neurological deficits, and ROS.
• NBOT increased adenosine triphosphate (ATP) production in ischemic rats.
• NBOT decreased transcriptional and translational levels of GLUT1/3, PFK1, and LDH.
• NBOT reduced both mRNA and protein expression of AMPK.

Conclusions:

• NBOT exhibits neuroprotective effects in ischemic stroke.
• NBOT mitigates hyperglycolysis by modulating the AMPK signaling pathway.
• NBOT alleviates oxidative injury, contributing to its therapeutic benefits.