Camelliasaponin B1, a saponin from Camellia oleifera seed, protects against oxidative stress by fine-tuning mitophagy via the BNIP3/NIX-LC3B pathway

Camelliasaponins, bioactive constituents abundant in the by-products of Camellia oleifera oil production, exhibit diverse biological activities. However, their potential in regulating neuroprotective mitophagy remains largely unexplored. This study identifies and investigates camelliasaponin B1 (CSB1) as an abundant component in the seeds of Camellia oleifera, validating its presence in this natural source and subsequently exploring its pharmacological activities at the cellular level. To explore its potential neuroprotective value, we established an in vitro model of H2O2-induced oxidative damage in PC12 cells. We found that CSB1 pretreatment alleviates oxidative stress and preserves mitochondrial function, as evidenced by the restoration of membrane potential , ultrastructure, and respiratory capacity. Mechanistically, CSB1 confers protection by suppressing excessive mitophagy through downregulation of the BNIP3/NIX-LC3B pathway. Our findings establish CSB1 as a multifaceted cytoprotective agent that enhances antioxidant defenses, safeguards mitochondrial integrity, and fine-tunes mitophagic flux, offering novel insights into its development as a high-value functional food ingredient.