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Updated: Aug 11, 2026
2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia
Published on: June 22, 2013
HBO suppresses Nogo-A, Ng-R, or RhoA expression in the cerebral cortex after global ischemia
Changman Zhou1, Yun Li, Anil Nanda
1Department of Neurosurgery, Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA, USA.
Abstract:
Nogo-A, a myelin-associated neurite outgrowth inhibitory protein, binds with the Ng-R receptor to activate RhoA intracellular signals and inhibit the plasticity after CNS injury. We evaluated the effect of hyperbaric oxygen (HBO) on the expression of Nogo-A, Ng-R, and RhoA after transient global ischemia in a rat 2 vessel occlusion global ischemic model. Male SD rats (n=78) were randomly divided into 13 groups: 1 sham group, 6 groups of global ischemia, and 6 groups of HBO treatment after global ischemia. HBO (3ATA) was applied for 2 hr at 1 hr after global ischemia. Rats were sacrificed at 6, 12, 24, 48, and 96 hr and 7 days. Global ischemia (10 min) produced a marked increase of Nogo-A/B, Nogo-A, Ng-R, and RhoA expression. Immunohistochemistry showed increased Nogo-A/B and Nogo-A located in the myelin sheath of ischemic brain cortex. Ng-R expressed on the surface of neurons and their processes, and RhoA expressed inside the cytoplasm of neurons in ischemic brain. HBO significantly reduced neurological injury, decreased the levels of Nogo-A, Ng-R, and RhoA in ischemic injured cortex (p<0.05).
Insights
Hyperbaric oxygen therapy (HBO) reduced neurological injury after global ischemia in rats. HBO therapy decreased the expression of Nogo-A, Ng-R, and RhoA, key inhibitors of neural plasticity.
Area of Science:
- Neuroscience
- Cellular Biology
- Ischemic Stroke Research
Background:
- Nogo-A, a neurite outgrowth inhibitor, binds Ng-R to activate RhoA, inhibiting plasticity post-CNS injury.
- Understanding Nogo-A pathway modulation is crucial for developing therapeutic strategies for ischemic brain injury.
Purpose of the Study:
- To investigate the effect of hyperbaric oxygen (HBO) on Nogo-A, Ng-R, and RhoA expression following transient global ischemia in a rat model.
- To assess HBO's potential to mitigate neurological deficits by modulating inhibitory pathways.
Main Methods:
- A rat model of transient global ischemia (2-vessel occlusion) was utilized with 78 male SD rats.
- Rats were divided into sham, ischemia, and HBO treatment groups, with HBO applied at 3ATA for 2 hours post-ischemia.
- Expression levels of Nogo-A/B, Nogo-A, Ng-R, and RhoA were analyzed via immunohistochemistry at various time points (6-96 hours and 7 days).
Main Results:
- Global ischemia significantly increased the expression of Nogo-A/B, Nogo-A, Ng-R, and RhoA in the ischemic brain cortex.
- Immunohistochemistry confirmed increased Nogo-A/B and Nogo-A in myelin sheaths and Ng-R and RhoA in neurons.
- HBO treatment significantly reduced neurological injury and decreased the expression of Nogo-A, Ng-R, and RhoA in the ischemic cortex (p<0.05).
Conclusions:
- Transient global ischemia upregulates the Nogo-A/Ng-R/RhoA pathway, contributing to inhibited neural plasticity.
- Hyperbaric oxygen therapy demonstrates a neuroprotective effect by downregulating this inhibitory pathway.
- HBO therapy holds promise as a therapeutic intervention for ischemic brain injury by promoting neural recovery.
