This study investigated the reparative effects of Brassica rapa L. ethanolic extract (BREE) on H 2 O 2 -induced oxidative injury in PC-12 cells. Brassica rapa L. , a cruciferous plant rich in bioactive flavonoids, exhibits potent antioxidant and neuroprotective properties against oxidative stress, a key pathological driver in neurodegenerative diseases. This study investigated the reparative effects of Brassica rapa L. ethanolic extract (BREE) on H 2 O 2 -induced oxidative injury in PC-12 cells, employing a multi-omics approach integrating LC-MS/MS metabolite profiling, molecular docking, and transcriptomic validation. BREE demonstrated robust radical-scavenging activity. Molecular docking identified direct interactions among flavonoids within BREE, suggesting a role in redox modulation. Subsequent experiments confirmed the activation of the PI3K/Akt, Keap1-Nrf2, and cell cycle pathways. Functionally, BREE significantly restored cell viability to 162.3% ± 6.9% of that in the control group. These findings validate BREE's dual action in scavenging ROS and reprogramming redox signaling networks, positioning it as a candidate for combating oxidative stress-associated neurodegeneration and as a potential functional food for age-related cognitive decline. • Integrating LC-MS metabolomics, transcriptomics, and molecular docking to study bioactives. • Revealed BREE's dual action in scavenging ROS and reprogramming redox signaling pathways. • We validated BREE's function to restored H 2 O 2 -injured PC-12 cell viability. • Findings position BREE as a candidate for mitigating age-related cognitive decline.
Wan et al. (Mon,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: