Targeted molecular docking-guided insights into the antioxidant reparative mechanisms of <i>Brassica rapa L.</i> extract after H<sub>2</sub>O<sub>2</sub>-induced neurotoxicity in PC-12 cells: Integration of LC-MS metabolomics and transcriptomic responses.

Abstract

This study investigated the reparative effects of <i>Brassica rapa L.</i> ethanolic extract (BREE) on H₂O₂-induced oxidative injury in PC-12 cells. <i>Brassica rapa L.</i>, 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 <i>Brassica rapa L.</i> ethanolic extract (BREE) on H₂O₂-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.