Lycium ruthenicum Murray anthocyanins alleviate neuroinflammation in MPTP-induced Parkinson's disease by modulating gut microbiota and tryptophan metabolism.

Parkinson's disease (PD) is closely linked to neuroinflammation, gut microbiota dysbiosis, and disrupted tryptophan metabolism, yet dietary interventions capable of coordinately targeting these processes remain insufficiently defined. Lycium ruthenicum Murray anthocyanins (LRA), a major bioactive component of black goji berry, have antioxidant and anti-inflammatory activities, but their gut microbiota-mediated neuroprotective mechanism in PD remains unclear. Here, we established a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model and treated mice with different doses of LRA. Behavioral tests, inflammatory and oxidative stress assays, Western blotting, 16S ribosomal RNA gene sequencing, and targeted metabolomic analysis were integrated to evaluate the effects of LRA. LRA improved motor dysfunction, exploratory behavior, and cognitive impairment in MPTP-induced PD mice, accompanied by reduced inflammatory cytokines and oxidative stress and partial restoration of striatal neurotrophic and dopaminergic markers. Moreover, LRA reshaped the gut microbiota, particularly by restoring Lachnospiraceae_NK4A136_group, unclassified_f__Lachnospiraceae, and Parabacteroides, and shifted tryptophan metabolism toward serotonin and indole derivatives, including indole-3-lactic acid, indole-3-acetic acid, and indole-3-propionic acid, while reducing quinolinic acid and xanthurenic acid. These findings suggest that LRA may improve PD-related neuroinflammation through a potential gut microbiota-tryptophan metabolism-neuroprotection axis.