Protective and restorative effects of magnolol on neurotoxicity in mice with 6-hydroxydopamine-induced hemiparkinsonism

Neurodegener Dis. 2011;8(5):364-74. doi: 10.1159/000323872. Epub 2011 Apr 15.


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 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.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biphenyl Compounds / administration & dosage*
  • Corpus Striatum / drug effects
  • Corpus Striatum / enzymology
  • Corpus Striatum / pathology
  • Disease Models, Animal*
  • Drug Administration Schedule
  • Lignans / administration & dosage*
  • Male
  • Mice
  • Neuroprotective Agents / administration & dosage*
  • Oxidopamine / antagonists & inhibitors
  • Oxidopamine / toxicity*
  • Parkinsonian Disorders / chemically induced
  • Parkinsonian Disorders / metabolism
  • Parkinsonian Disorders / prevention & control*
  • Tyrosine 3-Monooxygenase / antagonists & inhibitors
  • Tyrosine 3-Monooxygenase / metabolism


  • Biphenyl Compounds
  • Lignans
  • Neuroprotective Agents
  • magnolol
  • Oxidopamine
  • Tyrosine 3-Monooxygenase