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Article: Baicalin can scavenge peroxynitrite and ameliorate endogenous peroxynitrite-mediated neurotoxicity in cerebral ischemia-reperfusion injury

TitleBaicalin can scavenge peroxynitrite and ameliorate endogenous peroxynitrite-mediated neurotoxicity in cerebral ischemia-reperfusion injury
Authors
Issue Date2013
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/jethpharm
Citation
Journal of Ethnopharmacology, 2013, v. 150 n. 1, p. 116-124 How to Cite?
AbstractETHNOPHARMACOLOGICAL RELEVANCE: Baicalin is one of the principal flavonoids isolated from the dried root of Scutellaria baicalensis Georgi that has long been used to treat ischemic stroke. However, its neuroprotective mechanisms against cerebral ischemia injury are poorly understood. AIM OF THE STUDY: To explore the neuroprotective mechanisms of baicalin against cerebral ischemia reperfusion injury. MATERIAL AND METHODS: In chemical systems, we conducted electron paramagnetic resonance (EPR) spin trapping experiments to evaluate the scavenging effects of baicalin on superoxide and nitric oxide, and mass spectrometry (MS) studies on the reaction of baicalin and peroxynitrite. In cellular experiments, we investigated the effects of baicalin against extraneous and endogenous peroxynitrite mediated neurotoxicity in SH-SY5Y cells treated with peroxynitrite donor, synthesized peroxynitrite and exposed to oxygen glucose deprivation and reoxygenation (OGD/RO) in vitro. Moreover, we studied the neuroprotective effects of baicalin by using a rat model of middle cerebral artery occlusion in vivo. FeTMPyP, a peroxynitrite decomposition catalyst, was used as positive control. Cell viability and apoptotic cell death was accessed by MTT assay and TUNEL assay respectively; 3-nitrotyrosine formation and infarction volume were detected by immunostaining experiments and TTC staining respectively. RESULTS: Baicalin revealed strong antioxidant ability by directly scavenging superoxide and reacting with peroxynitrite. Baicalin protected the neuronal cells from extraneous and endogenous peroxynitrite-induced neurotoxicity. In ischemia-reperfused brains, baicalin inhibited the formation of 3-nitrotyrosine, reduced infarct size and attenuated apoptotic cell death, whose effects were similar to FeTMPyP. CONCLUSIONS: Baicalin can directly scavenge peroxynitrite and the peroxynitrite-scavenging ability contributes to its neuroprotective mechanisms against cerebral ischemia reperfusion injury.
Persistent Identifierhttp://hdl.handle.net/10722/195659
ISSN
2015 Impact Factor: 3.055
2015 SCImago Journal Rankings: 1.156
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorXu, Men_US
dc.contributor.authorChen, Xen_US
dc.contributor.authorGu, Yen_US
dc.contributor.authorPeng, Ten_US
dc.contributor.authorYang, Den_US
dc.contributor.authorChang, RCCen_US
dc.contributor.authorSo, KFen_US
dc.contributor.authorLiu, Ken_US
dc.contributor.authorShen, Jen_US
dc.date.accessioned2014-03-07T04:20:59Z-
dc.date.available2014-03-07T04:20:59Z-
dc.date.issued2013en_US
dc.identifier.citationJournal of Ethnopharmacology, 2013, v. 150 n. 1, p. 116-124en_US
dc.identifier.issn0378-8741en_US
dc.identifier.urihttp://hdl.handle.net/10722/195659-
dc.description.abstractETHNOPHARMACOLOGICAL RELEVANCE: Baicalin is one of the principal flavonoids isolated from the dried root of Scutellaria baicalensis Georgi that has long been used to treat ischemic stroke. However, its neuroprotective mechanisms against cerebral ischemia injury are poorly understood. AIM OF THE STUDY: To explore the neuroprotective mechanisms of baicalin against cerebral ischemia reperfusion injury. MATERIAL AND METHODS: In chemical systems, we conducted electron paramagnetic resonance (EPR) spin trapping experiments to evaluate the scavenging effects of baicalin on superoxide and nitric oxide, and mass spectrometry (MS) studies on the reaction of baicalin and peroxynitrite. In cellular experiments, we investigated the effects of baicalin against extraneous and endogenous peroxynitrite mediated neurotoxicity in SH-SY5Y cells treated with peroxynitrite donor, synthesized peroxynitrite and exposed to oxygen glucose deprivation and reoxygenation (OGD/RO) in vitro. Moreover, we studied the neuroprotective effects of baicalin by using a rat model of middle cerebral artery occlusion in vivo. FeTMPyP, a peroxynitrite decomposition catalyst, was used as positive control. Cell viability and apoptotic cell death was accessed by MTT assay and TUNEL assay respectively; 3-nitrotyrosine formation and infarction volume were detected by immunostaining experiments and TTC staining respectively. RESULTS: Baicalin revealed strong antioxidant ability by directly scavenging superoxide and reacting with peroxynitrite. Baicalin protected the neuronal cells from extraneous and endogenous peroxynitrite-induced neurotoxicity. In ischemia-reperfused brains, baicalin inhibited the formation of 3-nitrotyrosine, reduced infarct size and attenuated apoptotic cell death, whose effects were similar to FeTMPyP. CONCLUSIONS: Baicalin can directly scavenge peroxynitrite and the peroxynitrite-scavenging ability contributes to its neuroprotective mechanisms against cerebral ischemia reperfusion injury.en_US
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/jethpharm-
dc.relation.ispartofJournal of Ethnopharmacologyen_US
dc.titleBaicalin can scavenge peroxynitrite and ameliorate endogenous peroxynitrite-mediated neurotoxicity in cerebral ischemia-reperfusion injuryen_US
dc.typeArticleen_US
dc.identifier.emailPeng, T: pengtao@hku.hken_US
dc.identifier.emailYang, D: yangdan@hku.hken_US
dc.identifier.emailChang, RCC: rccchang@hku.hken_US
dc.identifier.emailSo, KF: hrmaskf@hku.hken_US
dc.identifier.emailShen, J: shenjg@hku.hken_US
dc.identifier.authorityYang, D=rp00825en_US
dc.identifier.authorityChang, RCC=rp00470en_US
dc.identifier.authoritySo, KF=rp00329en_US
dc.identifier.doi10.1016/j.jep.2013.08.020en_US
dc.identifier.pmid23973788-
dc.identifier.hkuros228224en_US
dc.identifier.volume150en_US
dc.identifier.issue1en_US
dc.identifier.spage116en_US
dc.identifier.epage124en_US
dc.identifier.isiWOS:000326998400011-
dc.publisher.placeIreland-

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