Abstract: In this study, an Aβ_25-35-induced PC12 cell damage model was established to investigate the neuroprotective effects and underlying mechanisms of aged Liupao tea (ALPT), with green tea (GT) as a reference. The results show that Aβ_25-35 significantly reduced PC12 cell viability, induced mitochondrial dysfunction, and promoted the formation of toxic aggregates and related pathways. ALPT markedly improved cell survival, increased mitochondrial membrane potential, and significantly inhibited the accumulation of toxic aggregates and the formation of related pathways. Furthermore, transcriptome analysis reveals that the overall gene expression pattern in the ALPT treatment group was the opposite to that in the Aβ_25-35 group, with upregulated genes involved in mitophagy, glycolysis and glycerophospholipid metabolism, and downregulated genes associated with cell cycle regulation, ribosomal function, ubiquitin-mediated proteolysis and cellular senescence. Overall, both GT and ALPT exhibited significant protective effects against Aβ_25-35-induced PC12 cell damage, though transcriptomic differences suggest that ALPT may have superior bioavailability due to its active components. This study provided experimental evidence for the potential application of ALPT in the prevention and treatment of neurodegenerative diseases.

Key words: aged Liupao tea, Aβ_25-35, PC12 cells, neuroprotective, mitochondrial function