SCOPE: Disruption of the blood-brain barrier (BBB) is a major pathogenic mechanism of neurological dysfunction and death after ischemic stroke. The aim of our study was to investigate the effect of procyanidin B2 (PB), a bioactive food compound, on BBB disruption induced by ischemic stroke and explore the underlying mechanism. METHODS AND RESULTS: PB was administrated intragastrically once a day starting at 3 h after transient middle cerebral artery occlusion (MCAO). PB treatment significantly decreased the infarction volume, brain edema, and neurological deficits after MCAO. PB prevented BBB disruption against ischemic stroke, as indicated by the reduction of Evans blue leakage and IgG levels. These results were also corroborated by immunofluorescence staining and Western blot analysis of ZO-1. Additionally, levels of reactive oxygen species and malondialdehyde were lessened in the ipsilateral ischemic area of brain by PB. The activities of antioxidant enzymes were elevated. Meanwhile, PB reversed the suppression of NF-E2-related factor nuclear translocation, and increased the protein expression of HO-1, GSTα, and NQO1 in the ipsilateral ischemic area of brain. CONCLUSION: PB attenuates neurological deficits and BBB disruption in a rat model of cerebral ischemia, and the neuroprotection of PB is associated with activation of NF-E2-related factor pathway.
SCOPE: Disruption of the blood-brain barrier (BBB) is a major pathogenic mechanism of neurological dysfunction and death after ischemic stroke. The aim of our study was to investigate the effect of procyanidin B2 (PB), a bioactive food compound, on BBB disruption induced by ischemic stroke and explore the underlying mechanism. METHODS AND RESULTS:PB was administrated intragastrically once a day starting at 3 h after transient middle cerebral artery occlusion (MCAO). PB treatment significantly decreased the infarction volume, brain edema, and neurological deficits after MCAO. PB prevented BBB disruption against ischemic stroke, as indicated by the reduction of Evans blue leakage and IgG levels. These results were also corroborated by immunofluorescence staining and Western blot analysis of ZO-1. Additionally, levels of reactive oxygen species and malondialdehyde were lessened in the ipsilateral ischemic area of brain by PB. The activities of antioxidant enzymes were elevated. Meanwhile, PB reversed the suppression of NF-E2-related factor nuclear translocation, and increased the protein expression of HO-1, GSTα, and NQO1 in the ipsilateral ischemic area of brain. CONCLUSION:PB attenuates neurological deficits and BBB disruption in a rat model of cerebral ischemia, and the neuroprotection of PB is associated with activation of NF-E2-related factor pathway.