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    題名: Protective and restorative effects of magnolol on neurotoxicity in mice with 6-hydroxydopamine-induced hemiparkinsonism
    作者: 詹銘煥
    Lin,Shiau-Chin;Chen,Hwei-Hsien;Chan,Ming-Huan
    日期: 2011.04
    上傳時間: 2012-11-14 13:43:14 (UTC+8)
    摘要: 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.
    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.
    關聯: Neurodegenerative Diseases, 8(5), 364-374
    資料類型: article
    顯示於類別:[神經科學研究所] 期刊論文

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