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Updated: Aug 6, 2025
A Murine Model of Ischemic Retinal Injury Induced by Transient Bilateral Common Carotid Artery Occlusion
Published on: November 12, 2020
TGF-β1 ameliorates BBB injury and improves long-term outcomes in mice after ICH
Huimei Wen1, Jiaying Tan1, Mi Tian1
1Department of Critical Care Medicine and Neurosurgery of Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, China.
Intracerebral hemorrhage (ICH) is a devastating subtype of stroke characterized by high mortality and morbidity rates with no effective treatment. TGF-β/ALK-5 signaling is reported to participated in the regulation of blood-brain barrier (BBB) integrity in the inflammation pain model, the effects of transforming growth factor (TGF)-β1 and the potential mechanisms on BBB after ICH have not been fully elucidated. Herein, we have demonstrated that peripheral administration of TGF-β1 reduces brain edema and ameliorated BBB injury after ICH. Consistent with previous results, TGF-β1 is shown to promote activation of anti-inflammatory microglia and reduce the inflammatory response after ICH. Furthermore, TGF-β1 administration improves long-term outcomes after ICH. Our data suggest that TGF-β1 may be a promising therapeutic agent for ICH.
Intracerebral hemorrhage (ICH) is a devastating subtype of stroke characterized by high mortality and morbidity rates with no effective treatment. TGF-β/ALK-5 signaling is reported to participated in the regulation of blood-brain barrier (BBB) integrity in the inflammation pain model, the effects of transforming growth factor (TGF)-β1 and the potential mechanisms on BBB after ICH have not been fully elucidated. Herein, we have demonstrated that peripheral administration of TGF-β1 reduces brain edema and ameliorated BBB injury after ICH. Consistent with previous results, TGF-β1 is shown to promote activation of anti-inflammatory microglia and reduce the inflammatory response after ICH. Furthermore, TGF-β1 administration improves long-term outcomes after ICH. Our data suggest that TGF-β1 may be a promising therapeutic agent for ICH.
