Please use this identifier to cite or link to this item:
https://ah.lib.nccu.edu.tw/handle/140.119/7653
DC Field | Value | Language |
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dc.creator | 詹銘煥 | zh_TW |
dc.creator | Lin,Shiau-Chin;Chen,Hwei-Hsien;Chan,Ming-Huan | - |
dc.date | 2011.04 | en_US |
dc.date.accessioned | 2012-11-14T05:43:14Z | - |
dc.date.available | 2012-11-14T05:43:14Z | - |
dc.date.issued | 2012-11-14T05:43:14Z | - |
dc.identifier.uri | https://nccur.lib.nccu.edu.tw/handle/140.119/7653 | - |
dc.description.abstract | Parkinson`s disease (PD) is one of the most common neurodegenerative disorders. The aim of the present study was to investigate the protective and restorative potential of magnolol, a major bioactive biphenolic from the bark of Magnolia officinalis, for alleviating the motor deficits induced by 6-hydroxydopamine (6-OHDA) in a mouse model of PD. Before or after unilateral striatal 6-OHDA lesion induction, mice were administered magnolol subchronically; then the apomorphine-induced rotational behaviors of the hemiparkinsonian mice and tyrosine hydroxylase (TH) expression in striatum were determined. Magnolol that was administered 30 min before 6-OHDA lesion induction and then applied daily for 14 days significantly ameliorated apomorphine-induced contralateral rotation in 6-OHDA-lesioned mice, and consistently protected the decreased levels of TH protein expression in striatum. One week after termination of the 7-day subchronic pretreatment, magnolol also remarkably prevented the dopaminergic neuronal loss as dentified by TH immunohistochemistry staining in striatum, associated with rotational behavioral protection in 6-OHDA-lesioned mice. Importantly, daily subchronic posttreatment with magnolol for 14 days efficiently reduced apomorphine-induced rotation, but did not restore the neuronal impairment in striatum damaged by 6-OHDA. Taken together, these findings suggest that magnolol may possess neuronal protective activity and behavioral restoration against 6-OHDA-induced toxicity in the PD model.Copyright © 2011 S. Karger AG, Basel. | - |
dc.description.abstract | Parkinson`s disease (PD) is one of the most common neurodegenerative disorders. The aim of the present study was to investigate the protective and restorative potential of magnolol, a major bioactive biphenolic from the bark of Magnolia officinalis, for alleviating the motor deficits induced by 6-hydroxydopamine (6-OHDA) in a mouse model of PD. Before or after unilateral striatal 6-OHDA lesion induction, mice were administered magnolol subchronically; then the apomorphine-induced rotational behaviors of the hemiparkinsonian mice and tyrosine hydroxylase (TH) expression in striatum were determined. Magnolol that was administered 30 min before 6-OHDA lesion induction and then applied daily for 14 days significantly ameliorated apomorphine-induced contralateral rotation in 6-OHDA-lesioned mice, and consistently protected the decreased levels of TH protein expression in striatum. One week after termination of the 7-day subchronic pretreatment, magnolol also remarkably prevented the dopaminergic neuronal loss as dentified by TH immunohistochemistry staining in striatum, associated with rotational behavioral protection in 6-OHDA-lesioned mice. Importantly, daily subchronic posttreatment with magnolol for 14 days efficiently reduced apomorphine-induced rotation, but did not restore the neuronal impairment in striatum damaged by 6-OHDA. Taken together, these findings suggest that magnolol may possess neuronal protective activity and behavioral restoration against 6-OHDA-induced toxicity in the PD model. | - |
dc.format | application/ | en_US |
dc.language | zh-TW | en_US |
dc.language | en-US | en_US |
dc.language.iso | en_US | - |
dc.relation | Neurodegenerative Diseases, 8(5), 364-374 | en_US |
dc.title | Protective and restorative effects of magnolol on neurotoxicity in mice with 6-hydroxydopamine-induced hemiparkinsonism | en_US |
dc.type | article | en |
item.grantfulltext | open | - |
item.openairetype | article | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | With Fulltext | - |
item.languageiso639-1 | en_US | - |
item.cerifentitytype | Publications | - |
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