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Gut microbiota regulation by Lactiplantibacillus plantarum SG5 enhances mitochondrial function in Parkinson's disease mice via the GLP-1/PGC-1α pathway
Lactiplantibacillus plantarum SG5 improves gut bacteria and boosts energy production in cells of Parkinson’s disease mice through the GLP-1/PGC-1α pathway
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Abstract
Supplementation with Lactiplantibacillus plantarum SG5 significantly alleviated motor deficits and dopaminergic neuron damage in Parkinson's disease mice.
- MPTP induced motor impairments and damage to dopaminergic neurons in male C57BL/6 mice aged 6-8 weeks.
- MPTP exposure resulted in mitochondrial dysfunction, decreased mitochondrial biogenesis, disrupted dynamics, and increased apoptosis.
- SG5 supplementation enhanced mitochondrial quality by increasing PGC-1α expression and restoring biogenesis, dynamics, and autophagy levels.
- SG5 increased colonic GLP-1 expression, suggesting a potential regulatory role of GLP-1 in mitochondrial function.
- GLP-1 receptor antagonists and PGC-1α inhibitors diminished the protective effects of SG5, indicating their involvement in SG5's mechanism.
- SG5 also counteracted MPTP-induced alterations in gut microbial diversity, highlighting its role in gut health.
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