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Conference Paper: Protective effects of lycium barbarum polysaccharides on cerebral edema and blook-brain barrier disruption after ischemic stroke

TitleProtective effects of lycium barbarum polysaccharides on cerebral edema and blook-brain barrier disruption after ischemic stroke
Authors
Issue Date2011
PublisherSociety for Neuroscience.
Citation
The 2011 Annual Meeting of the Society for Neuroscience, Washington, D.C., 12-16 November 2011. In Abstract Book of Neuroscience, 2011, p. 735-736 How to Cite?
AbstractBACKGROUND: Ischemic stroke is a destructive cerebrovascular disease and one of the leading causes of death worldwide. The long term disability after stroke induces heavy burden both to the patients and the society. Yet, no effective neuroprotective agents are available. The polysaccharides extracted from the fruits of wolfberry, Lycium barbarum (LBP), showed neuroprotective and immune-modulative functions. We aim to evaluate the protective effects of LBP in experimental stroke using a focal cerebral ischemia/reperfusion (I/R) model. METHODS: C57BL/6N mice were subjected to 2 h of middle cerebral artery occlusion (MCAO) followed by 22 h of reperfusion. Prior to ischemia induction, animals were orally fed with either vehicle (PBS) or LBP daily for 7 days. Mice were evaluated for neurological deficits just before sacrifice. Brains were harvested for infarct size estimation, water content measurement and immunohistochemical analysis as well as Western blot experiments. Evans blue (EB) extravasation experiment was performed to determine blood-brain barrier (BBB) disruption after MCAO. RESULTS: LBP treatment significantly improved neurological scores and decreased infarct size, hemispheric swelling and water content as well as reduced EB extravasation. In addition, fewer apoptotic cells were identified in the LBP-treated brains by TUNEL assay. Immunoreactivity for aquaporin-4 and glial fibrillary acidic protein were also significantly decreased in LBP-treated brains. We further observed a reduction of nuclear factor-κB translocation and IκB expression after LBP treatment.CONCLUSION: Seven-day LBP pre-treatment effectively improved neurological deficits, decreased infarct size and cerebral edema as well as protected the brain from BBB disruption, aquaporin water channel up-regulation and glial activation. The protective effects of LBP might partially act through its anti-inflammatory effects. The present study suggests that LBP may be used as a preventive neuroprotectant for ischemic stroke.
DescriptionPoster Session 361 - Ischemia: Neuroprotection II: no. 361.01/DD13
Persistent Identifierhttp://hdl.handle.net/10722/146970

 

DC FieldValueLanguage
dc.contributor.authorYang, Den_US
dc.contributor.authorLi, SYen_US
dc.contributor.authorChang, RCCen_US
dc.contributor.authorSo, KFen_US
dc.contributor.authorWong, DSHen_US
dc.contributor.authorLo, ACYen_US
dc.date.accessioned2012-05-23T05:51:18Z-
dc.date.available2012-05-23T05:51:18Z-
dc.date.issued2011en_US
dc.identifier.citationThe 2011 Annual Meeting of the Society for Neuroscience, Washington, D.C., 12-16 November 2011. In Abstract Book of Neuroscience, 2011, p. 735-736en_US
dc.identifier.urihttp://hdl.handle.net/10722/146970-
dc.descriptionPoster Session 361 - Ischemia: Neuroprotection II: no. 361.01/DD13-
dc.description.abstractBACKGROUND: Ischemic stroke is a destructive cerebrovascular disease and one of the leading causes of death worldwide. The long term disability after stroke induces heavy burden both to the patients and the society. Yet, no effective neuroprotective agents are available. The polysaccharides extracted from the fruits of wolfberry, Lycium barbarum (LBP), showed neuroprotective and immune-modulative functions. We aim to evaluate the protective effects of LBP in experimental stroke using a focal cerebral ischemia/reperfusion (I/R) model. METHODS: C57BL/6N mice were subjected to 2 h of middle cerebral artery occlusion (MCAO) followed by 22 h of reperfusion. Prior to ischemia induction, animals were orally fed with either vehicle (PBS) or LBP daily for 7 days. Mice were evaluated for neurological deficits just before sacrifice. Brains were harvested for infarct size estimation, water content measurement and immunohistochemical analysis as well as Western blot experiments. Evans blue (EB) extravasation experiment was performed to determine blood-brain barrier (BBB) disruption after MCAO. RESULTS: LBP treatment significantly improved neurological scores and decreased infarct size, hemispheric swelling and water content as well as reduced EB extravasation. In addition, fewer apoptotic cells were identified in the LBP-treated brains by TUNEL assay. Immunoreactivity for aquaporin-4 and glial fibrillary acidic protein were also significantly decreased in LBP-treated brains. We further observed a reduction of nuclear factor-κB translocation and IκB expression after LBP treatment.CONCLUSION: Seven-day LBP pre-treatment effectively improved neurological deficits, decreased infarct size and cerebral edema as well as protected the brain from BBB disruption, aquaporin water channel up-regulation and glial activation. The protective effects of LBP might partially act through its anti-inflammatory effects. The present study suggests that LBP may be used as a preventive neuroprotectant for ischemic stroke.-
dc.languageengen_US
dc.publisherSociety for Neuroscience.-
dc.relation.ispartofAbstract Book of Neuroscienceen_US
dc.rightsAbstracts of Neuroscience. Copyright © Society for Neuroscience.-
dc.titleProtective effects of lycium barbarum polysaccharides on cerebral edema and blook-brain barrier disruption after ischemic strokeen_US
dc.typeConference_Paperen_US
dc.identifier.emailLi, SY: sukyeeli@hku.hken_US
dc.identifier.emailChang, RCC: rccchang@hku.hken_US
dc.identifier.emailSo, KF: hrmaskf@hku.hken_US
dc.identifier.emailWong, DSH: shdwong@hku.hken_US
dc.identifier.emailLo, ACY: amylo@hku.hken_US
dc.identifier.authorityChang, RCC=rp00470en_US
dc.identifier.authorityWong, DSH=rp00516en_US
dc.identifier.authorityLo, ACY=rp00425en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros199720en_US
dc.identifier.spage735-
dc.identifier.epage736-
dc.publisher.placeUnited States-
dc.description.otherThe 2011 Annual Meeting of the Society for Neuroscience, Washington, D.C., 12-16 November 2011. In Abstract Book of Neuroscience, 2011, p. 735-736-

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