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Updated: Aug 24, 2026
A Cell Culture Model for Studying the Role of Neuron-Glia Interactions in Ischemia
Published on: November 14, 2020
Early exercise intervention alleviates neuroinflammation after ischemic stroke by regulating GSK-3β/HK2-associated
Nai Li1,2,3, Ya Wei1,2,3, Hongyi Wu4,5
1Tianjin Medical University General Hospital, Department of Physical and Rehabilitation Medicine, No. 154 Anshan Road, Tianjin 300052, China.
Abstract:
Microglia-mediated inflammation plays a critical role in secondary brain injury following ischemic stroke. Glycogen synthase kinase-3β (GSK-3β) and hexokinase 2 (HK2) are involved in regulating microglial inflammatory responses and can promote the release of pro-inflammatory factors under ischemic and hypoxic conditions, thereby exacerbating brain damage. Early exercise intervention has been shown to improve post-stroke neuroinflammation, but whether it exerts this effect by modulating GSK-3β/HK2-associated inflammatory signaling in microglia remains unclear. This study aimed to investigate the effects of early exercise on microglial inflammation and the potential involvement of GSK-3β/HK2 signaling. A twenty-eight-day early exercise regimen was applied in a rat model of middle cerebral artery occlusion (MCAO), and complementary in vitro experiments were conducted using BV2 microglial cells under oxygen-glucose deprivation. Results demonstrated that early exercise significantly improved neurological outcomes and reduced brain tissue damage, accompanied by decreased expression of microglial pro-inflammatory factors (IL-6, TNF-α, CD86, and iNOS) and increased levels of anti-inflammatory factors (IL-10 and Arg1). In vitro, inhibition of GSK-3β in BV2 cells markedly alleviated inflammatory responses under hypoxic conditions. In conclusion, early exercise intervention can attenuate post-stroke neuroinflammation, potentially by modulating GSK-3β/HK2 signaling in microglia to regulate.
Insights
Early exercise reduces brain damage after stroke by calming microglial inflammation. This intervention may modulate glycogen synthase kinase-3β (GSK-3β) and hexokinase 2 (HK2) signaling pathways in microglia.
Area of Science:
- Neuroscience
- Cell Biology
- Immunology
Background:
- Microglia-driven inflammation is key in secondary brain injury post-ischemic stroke.
- Glycogen synthase kinase-3β (GSK-3β) and hexokinase 2 (HK2) influence microglial inflammatory responses and exacerbate stroke damage.
- The impact of early exercise on GSK-3β/HK2-mediated microglial signaling in stroke is not well understood.
Purpose of the Study:
- To investigate the effects of early exercise on microglial inflammation following ischemic stroke.
- To explore the potential involvement of GSK-3β/HK2 signaling in exercise-induced neuroprotection.
Main Methods:
- A 28-day early exercise regimen was implemented in a rat model of middle cerebral artery occlusion (MCAO).
- In vitro studies utilized BV2 microglial cells subjected to oxygen-glucose deprivation.
- Key inflammatory markers (IL-6, TNF-α, CD86, iNOS, IL-10, Arg1) and GSK-3β activity were assessed.
Main Results:
- Early exercise significantly improved neurological function and reduced brain tissue damage in MCAO rats.
- Exercise decreased pro-inflammatory factors (IL-6, TNF-α, CD86, iNOS) and increased anti-inflammatory factors (IL-10, Arg1) in microglia.
- Inhibition of GSK-3β in vitro attenuated inflammatory responses in microglial cells under hypoxic conditions.
Conclusions:
- Early exercise intervention effectively reduces post-stroke neuroinflammation.
- This neuroprotective effect may be mediated through the modulation of GSK-3β/HK2 signaling pathways in microglia.
- Targeting GSK-3β/HK2 signaling presents a potential therapeutic strategy for stroke recovery.
