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Published on: January 7, 2014
Neuroprotection by Paeoniflorin in the MPTP mouse model of Parkinson's disease
Meizhu Zheng1, Chunming Liu1, Yajun Fan2
1The Central Laboratory, Changchun Normal University, Changchun, Jilin, PR China.
Abstract:
Paeoniflorin (PF) is a major bioactive ingredient in Radix Paeonia alba roots that has low toxicity and has been shown to have neuroprotective effects. Our in vitro experiments suggested that PF affords a significant neuroprotective effect against MPP+-induced damage and apoptosis in PC12 cells through Bcl-2/Bax/caspase-3 pathway. The objectives of the present study were to explore the potential neuroprotective effect of PF in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-treated mouse model of Parkinson's disease (PD). Our results demonstrated that PF treatment ameliorated the behavioral deficits of "in spontaneous motor activity and latency to fall of the rotarod test", and reduced dopaminergic cell loss that were induced by MPTP in a dose-dependent manner in an in vivo model of PD. In addition, we found that treatment of PF protected dopaminergic neurons by preventing MPTP-induced decreases in striatal and substantia nigra dopaminergic transporter (DAT) and tyrosine hydroxylase (TH) protein levels, and by changing dopamine catabolism and inhibiting dopamine turnover. Furthermore, it was also associated with up-regulation of the Bcl-2/BAD ratio, and inhibition of the activation of caspase-9 and caspase-3. These results showed that PF promoted dopamine neuron survival in vivo due to the MAO-B inhibition, and the PI3K/Akt signaling pathway may have mediated the protection of PF against MPTP, suggesting that PF treatment might represent a neuroprotective treatment for PD.
Insights
Paeoniflorin (PF) demonstrates neuroprotective effects in Parkinson's disease models. It preserves dopaminergic neurons and improves motor function by inhibiting MAO-B and activating the PI3K/Akt pathway.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Paeoniflorin (PF) from Radix Paeonia alba exhibits neuroprotective properties.
- In vitro studies indicated PF protects against MPP+-induced apoptosis in PC12 cells via the Bcl-2/Bax/caspase-3 pathway.
Purpose of the Study:
- To investigate the in vivo neuroprotective effects of PF in a mouse model of Parkinson's disease (PD) induced by MPTP.
- To elucidate the mechanisms underlying PF's neuroprotection against MPTP toxicity.
Main Methods:
- MPTP-treated mice were administered varying doses of PF.
- Behavioral tests (spontaneous motor activity, rotarod) assessed motor function.
- Dopaminergic cell loss, DAT, TH protein levels, dopamine catabolism, and apoptosis markers (Bcl-2, BAD, caspase-9, caspase-3) were analyzed.
- MAO-B activity and PI3K/Akt signaling pathway were investigated.
Main Results:
- PF treatment dose-dependently ameliorated behavioral deficits and reduced dopaminergic neuron loss in MPTP-treated mice.
- PF prevented MPTP-induced decreases in striatal and substantia nigra DAT and TH levels.
- PF modulated dopamine catabolism, inhibited dopamine turnover, and regulated apoptosis-related proteins (increased Bcl-2/BAD ratio, inhibited caspase-9 and -3 activation).
- PF inhibited MAO-B activity and activated the PI3K/Akt pathway.
Conclusions:
- PF promotes in vivo survival of dopaminergic neurons in an MPTP-induced PD model.
- PF exerts neuroprotection through MAO-B inhibition and PI3K/Akt pathway activation.
- PF shows potential as a neuroprotective therapeutic agent for Parkinson's disease.
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