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Updated: Oct 12, 2025

Two-vessel Occlusion Mouse Model of Cerebral Ischemia-reperfusion
Published on: March 1, 2019
WITHDRAWN: Foxp3 attenuates cerebral ischemia/reperfusion injury through microRNA-150-5p-modified NCS1
Zhen Gu1, Yajie Li1, Liang Zhang2
1Department of Neurosurgery, The Affiliated Hospital of Yunnan University, Kunming, 650011, Yunnan, China.
Objective:
Cerebral ischemia/reperfusion injury (CI/RI) is a pathological process involving complicated molecular mechanisms. We investigated forkhead box P3 (Foxp3)-related mechanism in CI/RI with particular focus on microRNA (miR)-150-5p/nucleobase cation symporter-1 (NCS1) axis.
Methods:
A mouse model was constructed by middle cerebral artery occlusion (MCAO) method. Levels of Foxp3, miR-150-5p and NCS1 were assessed in brain tissues of MCAO mice. By determining the neurological behavior function, neurological deficits, brain tissue pathological characteristics, neuronal apoptosis, inflammatory factors, and oxidative stress-related factors, the functional role of Foxp3, miR-150-5p and NCS1 were evaluated in MCAO mice. The feedback loop was analyzed among Foxp3, miR-150-5p and NCS1.
Results:
The level of Foxp3 and NCS1 were reduced and that of miR-150-5p was augmented in MCAO mice. Foxp3 bound to miR-150-5p to target NCS1. Up-regulating Foxp3 or NCS1 or suppressing miR-150-5p improved neurological behavior function and neurological deficits, and reduced brain tissue pathological damage, neuronal apoptosis, inflammatory and oxidative stress reactions in MCAO mice. Silencing miR-150-5p or elevating NCS1 decreased Foxp3 silencing-mediated ischemic injury in MCAO mice.
Conclusion:
Foxp3 is neuroprotective in CI/RI through binding to miR-150-5p to promote NCS1 expression.
Insights
Forkhead box P3 (Foxp3) protects the brain from cerebral ischemia/reperfusion injury (CI/RI) by regulating microRNA-150-5p and nucleobase cation symporter-1 (NCS1). This pathway reduces neuronal damage and inflammation, improving neurological function after stroke.
Area of Science:
- Neuroscience
- Molecular Biology
- Pathology
Background:
- Cerebral ischemia/reperfusion injury (CI/RI) involves complex molecular pathways.
- The role of forkhead box P3 (Foxp3) in CI/RI is not fully understood.
- The microRNA-150-5p (miR-150-5p) and nucleobase cation symporter-1 (NCS1) axis is implicated in cellular processes.
Purpose of the Study:
- To investigate the role of Foxp3 in CI/RI.
- To elucidate the involvement of the miR-150-5p/NCS1 axis in CI/RI.
- To determine the regulatory relationship between Foxp3, miR-150-5p, and NCS1 in CI/RI.
Main Methods:
- A mouse model of cerebral ischemia/reperfusion injury was established using middle cerebral artery occlusion (MCAO).
- Levels of Foxp3, miR-150-5p, and NCS1 were measured in brain tissues.
- Neurological function, brain pathology, neuronal apoptosis, inflammation, and oxidative stress were assessed to evaluate the roles of Foxp3, miR-150-5p, and NCS1.
Main Results:
- Foxp3 and NCS1 levels decreased, while miR-150-5p levels increased in MCAO mice.
- Foxp3 directly targets NCS1 via miR-150-5p.
- Upregulating Foxp3 or NCS1, or downregulating miR-150-5p, ameliorated neurological deficits and reduced CI/RI-induced damage, apoptosis, inflammation, and oxidative stress.
Conclusions:
- Foxp3 exhibits neuroprotective effects in CI/RI.
- Foxp3 promotes NCS1 expression by interacting with miR-150-5p.
- Targeting the Foxp3/miR-150-5p/NCS1 pathway may offer therapeutic strategies for CI/RI.

