Lactobacillus plantarum DP189 Reduces α-SYN Aggravation in MPTP-Induced Parkinson's Disease Mice via Regulating Oxidative Damage, Inflammation, and Gut Microbiota Disorder

This study aimed to evaluate the attenuating effect of Lactobacillus plantarum DP189 on alpha-synuclein (alpha-SYN) aggregates in the substantia nigra (SN) of Parkinson's disease (PD) mice via 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced. Our results indicated that L. plantarum DP189 increased the levels of superoxide dismutase (SOD), glutathione peroxide (GSH-Px), and interleukin-10 (IL-10) and decreased the levels of malondialdehyde (MDA), reactive oxygen species (ROS), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and interleukin-1 beta (IL-1 beta). Moreover, L. plantarum DP189 reduced the alpha-SYN accumulation in SN. Mechanistically, L. plantarum DP189 activated the expression of nuclear factor erythroid 2-related factor (Nrf2)/ARE and PGC-1 alpha pathways and suppressed the NLRP3 inflammasome. Furthermore, fecal analysis showed that L. plantarum DP189 reshaped the gut microbiota in PD mice by reducing the number of pathogenic bacteria (Proteobacteria and Actinobacteria) and increased the abundance of probiotics (Lactobacillus and Prevotella). Our results suggested that L. plantarum DP189 could delay the neurodegeneration caused by the accumulation of alpha-SYN in the SN of PD mice via suppressing oxidative stress, repressing proinflammatory response, and modulating gut microbiota.

Automated summary

Lactobacillus plantarum DP189 alleviates alpha-synuclein (α-SYN) aggregates in the substantia nigra (SN) of Parkinson's disease (PD) mice through various mechanisms, including activating antioxidant and anti-inflammatory pathways, suppressing the expression of inflammasomes, and modulating gut microbiota. These findings suggest that L. plantarum DP189 has the potential therapeutic effect in mitigating neurodegeneration in PD.