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Article: Baicalin Attenuates Blood-Brain Barrier Disruption and Hemorrhagic Transformation and Improves Neurological Outcome in Ischemic Stroke Rats with Delayed t-PA Treatment: Involvement of ONOO−-MMP-9 Pathway

TitleBaicalin Attenuates Blood-Brain Barrier Disruption and Hemorrhagic Transformation and Improves Neurological Outcome in Ischemic Stroke Rats with Delayed t-PA Treatment: Involvement of ONOO−-MMP-9 Pathway
Authors
KeywordsBaicalin
Hemorrhagic transformation
Ischemic stroke
Natural compound
Peroxynitrite
Issue Date2017
PublisherSpringer New York LLC. The Journal's web site is located at http://www.springer.com/biomed/neuroscience/journal/12975
Citation
Translational Stroke Research, 2017, p. 1-15 How to Cite?
AbstractTissue plasminogen activator (t-PA) has a restrictive therapeutic window within 4.5 h after ischemic stroke with the risk of hemorrhagic transformation (HT) and neurotoxicity when it is used beyond the time window. In the present study, we tested the hypothesis that baicalin, an active compound of medicinal plant, could attenuate HT in cerebral ischemia stroke with delayed t-PA treatment. Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 4.5 h and then continuously received t-PA infusion (10 mg/kg) for 0.5 h and followed by 19-h reperfusion. Baicalin (50, 100, 150 mg/kg) was administrated via femoral vein at 4.5 h after MCAO cerebral ischemia. Delayed t-PA infusion significantly increased the mortality rate, induced HT, blood-brain barrier (BBB) damage, and apoptotic cell death in the ischemic brains and exacerbated neurological outcomes in cerebral ischemia-reperfusion rats at 24 h after MCAO cerebral ischemia. Co-treatment of baicalin significantly reduced the mortality rates, ameliorated the t-PA-mediated BBB disruption and HT. Furthermore, baicalin showed to directly scavenge peroxynitrite and inhibit MMP-9 expression and activity in the ischemic brains with the delayed t-PA treatment. Baicalin had no effect on the t-PA fibrinolytic function indicated by t-PA activity assay. Taken together, baicalin could attenuate t-PA-mediated HT and improve the outcomes of ischemic stroke treatment possibly via inhibiting peroxynitrite-mediated MMP-9 activation. © 2017 Springer Science+Business Media, LLC, part of Springer Nature
Persistent Identifierhttp://hdl.handle.net/10722/250508
ISSN
2017 Impact Factor: 8.266
2015 SCImago Journal Rankings: 1.311
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChen, H-
dc.contributor.authorGuan, B-
dc.contributor.authorChen, X-
dc.contributor.authorChen, X-
dc.contributor.authorLi, C-
dc.contributor.authorQiu, J-
dc.contributor.authorYang, D-
dc.contributor.authorLiu, K-
dc.contributor.authorQi, S-
dc.contributor.authorShen, J-
dc.date.accessioned2018-01-17T08:44:03Z-
dc.date.available2018-01-17T08:44:03Z-
dc.date.issued2017-
dc.identifier.citationTranslational Stroke Research, 2017, p. 1-15-
dc.identifier.issn1868-4483-
dc.identifier.urihttp://hdl.handle.net/10722/250508-
dc.description.abstractTissue plasminogen activator (t-PA) has a restrictive therapeutic window within 4.5 h after ischemic stroke with the risk of hemorrhagic transformation (HT) and neurotoxicity when it is used beyond the time window. In the present study, we tested the hypothesis that baicalin, an active compound of medicinal plant, could attenuate HT in cerebral ischemia stroke with delayed t-PA treatment. Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 4.5 h and then continuously received t-PA infusion (10 mg/kg) for 0.5 h and followed by 19-h reperfusion. Baicalin (50, 100, 150 mg/kg) was administrated via femoral vein at 4.5 h after MCAO cerebral ischemia. Delayed t-PA infusion significantly increased the mortality rate, induced HT, blood-brain barrier (BBB) damage, and apoptotic cell death in the ischemic brains and exacerbated neurological outcomes in cerebral ischemia-reperfusion rats at 24 h after MCAO cerebral ischemia. Co-treatment of baicalin significantly reduced the mortality rates, ameliorated the t-PA-mediated BBB disruption and HT. Furthermore, baicalin showed to directly scavenge peroxynitrite and inhibit MMP-9 expression and activity in the ischemic brains with the delayed t-PA treatment. Baicalin had no effect on the t-PA fibrinolytic function indicated by t-PA activity assay. Taken together, baicalin could attenuate t-PA-mediated HT and improve the outcomes of ischemic stroke treatment possibly via inhibiting peroxynitrite-mediated MMP-9 activation. © 2017 Springer Science+Business Media, LLC, part of Springer Nature-
dc.languageeng-
dc.publisherSpringer New York LLC. The Journal's web site is located at http://www.springer.com/biomed/neuroscience/journal/12975-
dc.relation.ispartofTranslational Stroke Research-
dc.rightsThe final publication is available at Springer via http://dx.doi.org/[insert DOI]-
dc.subjectBaicalin-
dc.subjectHemorrhagic transformation-
dc.subjectIschemic stroke-
dc.subjectNatural compound-
dc.subjectPeroxynitrite-
dc.titleBaicalin Attenuates Blood-Brain Barrier Disruption and Hemorrhagic Transformation and Improves Neurological Outcome in Ischemic Stroke Rats with Delayed t-PA Treatment: Involvement of ONOO−-MMP-9 Pathway-
dc.typeArticle-
dc.identifier.emailChen, H: chenhs@hku.hk-
dc.identifier.emailYang, D: yangdan@hku.hk-
dc.identifier.emailShen, J: shenjg@hku.hk-
dc.identifier.authorityYang, D=rp00825-
dc.identifier.authorityShen, J=rp00487-
dc.identifier.doi10.1007/s12975-017-0598-3-
dc.identifier.scopuseid_2-s2.0-85038835655-
dc.identifier.hkuros283982-
dc.identifier.spage1-
dc.identifier.epage15-
dc.identifier.isiWOS:000444426000009-
dc.publisher.placeUnited States-

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