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AimsParkinson's disease (PD) is a complex neurodegenerative disorder lacking disease-modifying therapies. This study aimed to systematically investigate the therapeutic potential and underlying mechanisms of Alpinetin in PD.MethodsAn integrated approach combining network pharmacology and molecular docking was employed to predict the core targets and pathways of Alpinetin in PD. These computational predictions were subsequently validated through in vivo animal experiments.ResultsNetwork pharmacology analysis predicted that Alpinetin exerts its effects by modulating mitophagy and dopaminergic synaptic pathways. Molecular docking revealed strong binding affinities between Alpinetin and key targets, including HIF1A, SQSTM1, and SRC. Guided by these findings, animal experiments confirmed the neuroprotective effects of Alpinetin, aligning with the predicted mechanisms.ConclusionOur findings demonstrate that Alpinetin has significant therapeutic potential for PD, likely mediated through the regulation of mitophagy and dopaminergic synapses. This study elucidates the molecular targets and mechanisms of Alpinetin, providing a solid foundation for its further investigation as an anti-PD agent.
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