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

Abstract

This study aimed to evaluate the attenuating effect of <i>Lactobacillus plantarum</i> DP189 on α-synuclein (α-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 <i>L. plantarum</i> 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-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β). Moreover, <i>L. plantarum</i> DP189 reduced the α-SYN accumulation in SN. Mechanistically, <i>L. plantarum</i> DP189 activated the expression of nuclear factor erythroid 2-related factor (Nrf2)/ARE and PGC-1α pathways and suppressed the NLRP3 inflammasome. Furthermore, fecal analysis showed that <i>L. plantarum</i> DP189 reshaped the gut microbiota in PD mice by reducing the number of pathogenic bacteria (<i>Proteobacteria</i> and <i>Actinobacteria</i>) and increased the abundance of probiotics (<i>Lactobacillus</i> and <i>Prevotella</i>). Our results suggested that <i>L. plantarum</i> DP189 could delay the neurodegeneration caused by the accumulation of α-SYN in the SN of PD mice via suppressing oxidative stress, repressing proinflammatory response, and modulating gut microbiota.