title: Procyanidin B2 attenuates neurological deficits and blood-brain barrier disruption in a rat model of cerebral ischemia.
abstract: METHODS
  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.
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Key Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, Wuhan University School of Pharmaceutical Sciences, Wuhan University, Wuhan, P. R. China.
authors.forename: Shuangchan
authors.initials: S
authors.lastname: Wu
authors.affiliation: Key Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, Wuhan University School of Pharmaceutical Sciences, Wuhan University, Wuhan, P. R. China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Yue
authors.affiliation: Key Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, Wuhan University School of Pharmaceutical Sciences, Wuhan University, Wuhan, P. R. China.
authors.forename: Jian
authors.initials: J
authors.lastname: Li
authors.affiliation: Key Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, Wuhan University School of Pharmaceutical Sciences, Wuhan University, Wuhan, P. R. China.
authors.forename: Zhike
authors.initials: Z
authors.lastname: Li
authors.affiliation: Key Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, Wuhan University School of Pharmaceutical Sciences, Wuhan University, Wuhan, P. R. China.
authors.forename: Xiaofei
authors.initials: X
authors.lastname: Li
authors.affiliation: Key Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, Wuhan University School of Pharmaceutical Sciences, Wuhan University, Wuhan, P. R. China.
authors.forename: Yunhui
authors.initials: Y
authors.lastname: Niu
authors.affiliation: Key Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, Wuhan University School of Pharmaceutical Sciences, Wuhan University, Wuhan, P. R. China.
authors.forename: Jin
authors.initials: J
authors.lastname: Xiang
authors.affiliation: Key Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, Wuhan University School of Pharmaceutical Sciences, Wuhan University, Wuhan, P. R. China.
authors.forename: Hong
authors.initials: H
authors.lastname: Ding
mesh_terms: D000818:Animals; D044946:Biflavonoids / Q000494:pharmacology*; D001812:Blood-Brain Barrier / Q000187:drug effects*; D001929:Brain Edema / Q000188:drug therapy / Q000473:pathology; D002545:Brain Ischemia / Q000188:drug therapy* / Q000503:physiopathology*; D002392:Catechin / Q000494:pharmacology*; D004195:Disease Models, Animal; D005982:Glutathione Transferase / Q000378:metabolism; D051547:Heme Oxygenase-1 / Q000378:metabolism; D008658:Inactivation, Metabolic / Q000187:drug effects; D020244:Infarction, Middle Cerebral Artery; D007527:Isoenzymes / Q000378:metabolism; D008297:Male; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects; D010539:Permeability / Q000187:drug effects; D044945:Proanthocyanidins / Q000494:pharmacology*; D017207:Rats, Sprague-Dawley; D019108:Tight Junctions / Q000187:drug effects / Q000473:pathology
chemical_list: D044946:Biflavonoids; D007527:Isoenzymes; D018696:Neuroprotective Agents; D044945:Proanthocyanidins; C479580:procyanidin B2; D002392:Catechin; D051547:Heme Oxygenase-1; D016660:NAD(P)H Dehydrogenase (Quinone); C507703:NQO1 protein, rat; D005982:Glutathione Transferase; C119995:glutathione S-transferase alpha
keywords: Blood-brain barrier; Ischemic stroke; Neurological deficits; Nrf2; Procyanidin B2