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Updated: Feb 15, 2026
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A Rat Model of Mild Intrauterine Hypoperfusion with Microcoil Stenosis
Published on: January 7, 2018
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Physical Exercise Improves Cognitive Function Together with Microglia Phenotype Modulation and Remyelination in
Ting Jiang1, Liying Zhang1, Xiaona Pan1
1Department of Rehabilitation Medicine, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Frontiers in Cellular Neuroscience
|January 10, 2018
Summary
Physical exercise enhances cognitive function and myelin repair in rats with chronic cerebral hypoperfusion. It promotes oligodendrocyte progenitor cell (OPC) differentiation and M2 microglia polarization via the CX3CL1/CX3CR1 axis.
Area of Science:
- Neuroscience
- Cell Biology
- Regenerative Medicine
Background:
- Myelin integrity is crucial for cognitive function and vulnerable to ischemic damage.
- Impaired oligodendrocyte progenitor cell (OPC) differentiation hinders remyelination in cerebrovascular diseases.
- Physical exercise shows potential for improving cognitive function, but its role in ischemic remyelination is unclear.
Purpose of the Study:
- To investigate the effects of physical exercise on cognitive function and remyelination following chronic cerebral hypoperfusion (CCH).
- To elucidate the underlying mechanisms, including OPCs behavior, microglia polarization, and molecular signaling pathways.
Main Methods:
- Rats underwent CCH via bilateral carotid artery occlusion.
- Physical exercise intervention was applied post-CCH.
- Evaluated cognitive function, myelin integrity, OPC proliferation/differentiation, microglia polarization (M1/M2), CX3CL1/CX3CR1 expression, and MAPK pathway activation (ERK, JNK).
Main Results:
- Physical exercise improved cognitive function and alleviated myelin injury in CCH rats.
- Exercise promoted OPC proliferation and differentiation, enhancing oligodendrocytegenesis.
- Exercise facilitated M2 microglia polarization and upregulated the CX3CL1/CX3CR1 axis, reducing ERK/JNK phosphorylation.
Conclusions:
- Physical exercise ameliorates cognitive deficits and promotes remyelination in CCH by modulating microglial phenotype and enhancing oligodendrocytegenesis.
- The CX3CL1/CX3CR1 axis is a key mediator in exercise-induced neuroprotection and remyelination, acting through ERK and JNK pathways.
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