TGF-β1 ameliorates BBB injury and improves long-term outcomes in mice after 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. •TGF-β1 attenuates blood-brain barrier damage and promotes long-term neurologic functional outcomes after ICH.•TGF-β1 modulates microglia activation and attenuated neutrophil infiltration after ICH.•TGF-β1 has no effect on the percentages of neutrophils and macrophages in the peripheral blood.