Abstract: Caenorhabditis eleganswas employed as a model organism to establish a Parkinson’s disease （PD） model by inducing dopaminergic neurodegeneration with 6-hydroxydopamine （6-OHDA）. This study investigated the effects of astaxanthin （AST） on oxidative stress, lipid metabolism, and dopaminergic neuron-mediated locomotion in PD worms, and utilized transcriptomic analysis to elucidate the underlying mechanisms. The results demonstrated that astaxanthin not only ameliorated oxidative stress, restored dopaminergic neuron function, improved locomotor capacity, and modulated lipid metabolism, but also exerted neuroprotective effects against 6-OHDA-induced toxicity by regulating the expression of key genes, includingCELE_F10D2.9, CELE_F38E1.5, andCELE_K08F4.6. These findings suggested that astaxanthin might serve as a potential therapeutic agent in PD by modulating specific genetic pathways.

Key words: astaxanthin, Parkinson’s disease nematode model, oxidative stress, transcriptome, neuroprotection