Parkinson’s disease (PD) is a progressive neurodegenerative disorder common in middle-aged and older adults, characterised by apoptosis of dopaminergic neurons in the substantia nigra, abnormal aggregation of α-synuclein, mitochondrial dysfunction, and chronic neuroinflammation, with a lack of clinical treatments targeting the underlying causes. Mitochondrial peptides from bovine embryonic brain cells contain 538 bioactive signalling molecules widely involved in neural development, mitochondrial energy metabolism, oxidative stress balance, inflammation regulation, and protein homeostasis degradation. This study used a network pharmacology approach, taking the 538 mitochondrial peptide molecules as the research material, to screen PD disease targets and identify overlapping peptide-disease targets; a protein-protein interaction (PPI) network was constructed and hub genes selected; GO function and KEGG pathway enrichment analyses were conducted; a peptide-target-pathway regulatory network was built; and molecular docking validated interactions between core peptides and hub targets, systematically illustrating the multi-target, multi-pathway molecular regulation mechanism by which bovine embryonic brain cell mitochondrial peptides may affect PD risk. The results showed a significant overlap of targets between mitochondrial peptides and PD, with PPI network analysis highlighting IL-7, IL-15, PDGFRA and other core hub genes; GO enrichment was mainly related to neuronal apoptosis regulation, oxidative stress response, mitochondrial structure assembly, and synaptic plasticity regulation; KEGG pathway enrichment focused on the Parkinson's disease pathway, oxidative phosphorylation, PI3K-AKT, MAPK, neuroinflammation, and autophagy-apoptosis pathways; molecular docking confirmed stable binding activity between core peptides and key PD targets. The study suggests that mitochondrial peptides from bovine embryonic brain cells may intervene in PD pathology by inhibiting neuroinflammation, repairing mitochondrial function, counteracting oxidative stress, regulating abnormal protein aggregation, protecting dopaminergic neurons, and balancing apoptosis and autophagy, providing a theoretical and molecular basis for nutritional intervention, mechanism research, and functional peptide development in PD.