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Updated: Jun 10, 2026
Primary Culture of Mouse Dopaminergic Neurons
Published on: September 8, 2014
Morin exerts neuroprotective actions in Parkinson disease models in vitro and in vivo
Zhen-tao Zhang1, Xue-bing Cao, Nian Xiong
1Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, China. zhangzhentao104@yahoo.com.cn
Aim:
To investigate the neuroprotective effects of morin on 1-methyl-4-phenylpyridinium ion (MPP(+))-induced apoptosis in neuronal differentiated PC12 cells as well as in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson disease (PD).
Methods:
PC12 cells were challenged with MPP(+) in the presence or absence of morin. Cell viability was determined using MTT assay. Cell apoptosis was measured using flow cytometry. Generation of reactive oxygen species (ROS) was assayed using fluorescence assay. In an MPTP mouse model of PD, behavioral deficits, striatal dopamine content, and number of dopaminergic neurons were measured.
Results:
MPP(+) induced apoptosis and ROS formation in PC12 cells. Concomitant treatment with morin (5-50 mumol/L) significantly attenuated the loss of cell viability and apoptosis when compared with MPP(+) treatment alone. Morin also attenuated ROS formation induced by MPP(+). MPTP induced permanent behavioral deficits and nigrostriatal lesions in mice. When administered prior to MPTP, morin (20 to 100 mg/kg) attenuated behavioral deficits, dopaminergic neuronal death and striatal dopamine depletion in the MPTP mouse model.
Conclusion:
The findings suggest that morin has neuroprotective actions both in vitro and in vivo, and may provide a novel therapeutic agent for the treatment of PD and other neurodegenerative diseases.
Insights
Morin demonstrates neuroprotective effects against 1-methyl-4-phenylpyridinium ion (MPP(+))-induced apoptosis in neuronal cells and in a mouse model of Parkinson disease (PD) by reducing cell death and reactive oxygen species.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Parkinson disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons.
- 1-methyl-4-phenylpyridinium ion (MPP(+)) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) are commonly used toxins to model PD in vitro and in vivo.
- Oxidative stress and apoptosis are key mechanisms implicated in PD pathogenesis.
Purpose of the Study:
- To evaluate the neuroprotective potential of morin against MPP(+)-induced apoptosis in PC12 cells.
- To assess the efficacy of morin in an MPTP-induced mouse model of Parkinson disease.
Main Methods:
- PC12 cells were treated with MPP(+) in the presence or absence of morin, with cell viability, apoptosis, and reactive oxygen species (ROS) measured.
- MPTP mouse model was used to evaluate behavioral deficits, striatal dopamine levels, and dopaminergic neuron survival.
- MTT assay, flow cytometry, and fluorescence assays were employed for in vitro analysis.
Main Results:
- MPP(+) exposure induced significant apoptosis and ROS generation in PC12 cells.
- Morin treatment dose-dependently reduced MPP(+)-induced cell death and ROS formation.
- In the MPTP mouse model, morin administration attenuated behavioral impairments, dopaminergic neurodegeneration, and dopamine depletion.
Conclusions:
- Morin exhibits significant neuroprotective properties in both cellular and animal models of Parkinson disease.
- These findings suggest morin's potential as a therapeutic agent for PD and other neurodegenerative conditions.
- Morin's mechanism involves the mitigation of oxidative stress and apoptosis.
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