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Published on: January 7, 2014
Ginsenoside Re exerts neuroprotective in MPTP mice: potential links to gut microbiota and serum metabolism
Jie Li1, Guijia Zhao1, Chunhui Yu1
1Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, 130117, PR China.
Abstract:
A Parkinson's disease (PD) model was established using male C57BL/6 mice administered 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), through which the neuroprotective effect of Ginsenoside Re (G-Re) was investigated. Although G-Re has demonstrated beneficial effects in MPTP-treated mice, its in vivo activity and the mechanisms underlying its therapeutic potential in PD remain insufficiently understood. In this study, microbiomics and metabolomics analyses were comprehensively employed to investigate gut microbial and metabolic changes in MPTP-induced mice following G-Re intervention, with the aim of elucidating G-Re's mechanisms of action in PD. G-Re administration was found to alleviate dyskinesia, attenuate dopaminergic neuronal loss, reduce alpha-synuclein aggregation, and enhance antioxidant defenses in MPTP-treated mice. Notably, G-Re significantly increased the relative abundance of Bifidobacterium, Clostridium, and Prevotella while decreasing the relative abundance of Akkermansia, Sutterella, and Allobaculum, thereby contributing to the restoration of gut microbiota composition. Non-targeted metabolomics revealed that G-Re exerted neuroprotective effects by modulating disruptions in the arachidonic acid, sphingolipid, and linoleic acid metabolic pathways, as well as pathways related to the biosynthesis of unsaturated fatty acids. Correlation analyses further demonstrated a significant association between specific gut microbes and the sphingolipid metabolic pathway. In addition, G-Re was found to inhibit pro-apoptotic proteins such as Bax and caspase-3 within the sphingolipid pathway while promoting the activity of anti-apoptotic proteins. Collectively, these findings provide both a scientific and theoretical basis supporting the therapeutic potential of G-Re in the treatment of PD.
Insights
Ginsenoside Re (G-Re) shows neuroprotective effects in Parkinson's disease (PD) models by restoring gut microbiota and modulating metabolic pathways. This study elucidates G-Re's therapeutic mechanisms, offering a scientific basis for its use in PD treatment.
Area of Science:
- Neuroscience
- Pharmacology
- Microbiology
Background:
- Parkinson's disease (PD) is a neurodegenerative disorder with limited treatment options.
- Ginsenoside Re (G-Re) shows potential therapeutic benefits in PD, but its mechanisms are not fully understood.
- Gut microbiota dysbiosis is implicated in PD pathogenesis.
Purpose of the Study:
- To investigate the neuroprotective effects and underlying mechanisms of Ginsenoside Re (G-Re) in a mouse model of Parkinson's disease (PD).
- To elucidate the impact of G-Re on gut microbiota composition and metabolic pathways in MPTP-induced PD mice.
Main Methods:
- Establishment of a Parkinson's disease (PD) mouse model using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).
- Administration of Ginsenoside Re (G-Re) to MPTP-treated mice.
- Comprehensive analysis using microbiomics and metabolomics.
- Assessment of motor function, dopaminergic neurodegeneration, alpha-synuclein aggregation, and antioxidant defenses.
- Correlation analysis between gut microbes and metabolic pathways.
Main Results:
- Ginsenoside Re (G-Re) alleviated motor deficits, protected dopaminergic neurons, reduced alpha-synuclein aggregation, and enhanced antioxidant capacity in MPTP-treated mice.
- G-Re modulated gut microbiota composition, increasing beneficial bacteria like Bifidobacterium and decreasing harmful bacteria.
- G-Re intervention normalized metabolic pathways, including arachidonic acid, sphingolipid, and linoleic acid metabolism.
- Specific gut microbes were significantly associated with the sphingolipid pathway, and G-Re modulated apoptosis-related proteins within this pathway.
Conclusions:
- Ginsenoside Re (G-Re) demonstrates significant neuroprotective effects in a Parkinson's disease (PD) model.
- G-Re's therapeutic potential in PD is mediated by restoring gut microbiota balance and modulating key metabolic pathways, particularly the sphingolipid pathway.
- These findings provide a scientific foundation for considering G-Re as a therapeutic agent for Parkinson's disease.
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