期刊
NEURODEGENERATIVE DISEASES
卷 8, 期 5, 页码 364-374出版社
KARGER
DOI: 10.1159/000323872
关键词
Apomorphine; Magnolol; 6-Hydroxydopamine; Parkinson's disease; Tyrosine hydroxylase
资金
- National Science Council, Taiwan [NSC97-2320-B-320-002-MY3]
Parkinson's disease (PD) is one of the most common neuro-degenerative 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 apo-morphine-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 identified 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 (C) 2011 S. Karger AG, Basel
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