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Published on: January 7, 2014
Curcumin Regulates Gut Microbiota and Exerts a Neuroprotective Effect in the MPTP Model of Parkinson's Disease
Hong Zhu1,2, Houwen Zhang1,2, Bonan Hou1,2
1Department of Neurology, The Second Affiliated Hospital of Zhejiang Chinese Medical University (Xinhua Hospital of Zhejiang Province), Hangzhou 310000, China.
Objectives:
The experiment aimed to explore the effects of curcumin on motor impairment, dopamine neurons, and gut microbiota in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mice model.
Methods:
Mice were randomly assigned to six groups: normal control group, solvent control group, MPTP group, curcumin-low-dose group (40 mg/kg), curcumin-medium-dose group (80 mg/kg), and curcumin-high-dose group (160 mg/kg). After 14 days, each group of mice was subjected to the pole text, the hanging test, and the open-field test. Tyrosine hydroxylase (TH) immunohistochemistry was used to observe the survival of nigrostriatal dopamine neurons. Moreover, ultrastructural changes were observed with a transmission electron microscope in mice striatal tissue cells. Then, 16S rRNA was used to assess changes in the gut microbiota.
Results:
(1) Each dose of curcumin reduced pole climbing time and increased suspension score and total distance moved dose-dependently. (2) All curcumin groups improved cell wrinkling and vacuolar degeneration, increased the number of TH positives, improved cell survival, and the higher the dose of curcumin, the better the effect. (3) There were differences in microbiota composition and a relative abundance among the groups. The relative abundance of Patescibacteria, Proteobacteria, and Verrucomicrobia was higher in the MPTP group. The relative abundance of Patescibacteria, Enterobacteriaceae, Enterococcaceae all decreased in all curcumin groups. In addition, the Kyoto Encyclopedia of Genes and Genomes pathways showed a reduction in the superpathway of N-acetylneuraminate degradation after medium- and high-dose curcumin administration.
Conclusions:
Curcumin regulates gut microbiota and exerts a neuroprotective effect in the MPTP mice model. This preliminary study demonstrates the therapeutic potential of curcumin for Parkinson's disease, providing clues for microbially targeted therapies for Parkinson's disease.
Insights
Curcumin treatment improved motor function and protected dopamine neurons in a mouse model of Parkinson's disease. It also modulated gut microbiota, suggesting therapeutic potential for Parkinson's disease.
Area of Science:
- Neuroscience
- Pharmacology
- Microbiology
Background:
- Parkinson's disease is characterized by motor impairment and loss of dopamine neurons.
- The gut microbiota is increasingly recognized as a factor influencing neurodegenerative diseases.
Purpose of the Study:
- To investigate the effects of curcumin on motor deficits, dopamine neuron survival, and gut microbiota composition in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced Parkinson's disease mouse model.
Main Methods:
- Mice were administered varying doses of curcumin or vehicle after MPTP exposure.
- Motor function was assessed using pole, hanging, and open-field tests.
- Dopamine neuron survival was evaluated via tyrosine hydroxylase (TH) immunohistochemistry, and gut microbiota changes were analyzed using 16S rRNA sequencing.
Main Results:
- Curcumin administration dose-dependently improved motor function, evidenced by reduced pole climbing time and increased suspension scores and movement distance.
- Curcumin treatment preserved nigrostriatal dopamine neurons, reducing cell damage and increasing TH-positive cells.
- Curcumin altered gut microbiota composition, decreasing the relative abundance of Patescibacteria, Proteobacteria, and Verrucomicrobia, and impacting microbial metabolic pathways.
Conclusions:
- Curcumin exhibits neuroprotective effects and modulates gut microbiota in an MPTP-induced Parkinson's disease model.
- These findings highlight curcumin's therapeutic potential for Parkinson's disease and suggest avenues for microbiota-targeted therapies.
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