The Extract of <i>Chrysanthemum morifolium Ramat.</i> Protects Conjunctival Epithelial Cells from Ultraviolet-Induced Damage in Vitro

Background Ultraviolet (UV) radiation threatens ocular surface integrity, while the involvement of ferroptosis—an iron-dependent, lipid peroxidation-driven cell death—in UV-induced conjunctival damage remains unexplored. Chrysanthemum morifolium extract (CME), a traditional herb with vision-protective properties, was evaluated for its potential to mitigate this damage. Methods Human conjunctival epithelial cells (HCoECs) were exposed to UV to model solar injury. CME was characterized and its effects were assessed through cell viability (CCK-8), lipid peroxidation (MDA assay), ROS production, and mRNA sequencing. Bioinformatic tools (eg, Swiss Target Prediction, STRING) identified flavonoid targets and ferroptosis-related networks. Results UV exposure triggered ferroptosis in HCoECs, evidenced by iron overload (TFRC1 upregulation), elevated ROS/MDA, and suppressed cell viability. RNA-seq revealed activation of ferroptosis pathways (eg, TFRC1, ACSL4) and inflammation signaling (eg, IL-17/HIF-1). CME pretreatment (100 μg/mL) significantly attenuated these effects, lowering MDA levels and restoring cell viability. Mechanistically, CME inhibited TFRC1-mediated iron influx and disrupted ferroptosis effector networks. Conclusion Our findings demonstrate that CME could protect HCoECs from UV-induced ferroptosis by chelating iron and suppressing lipid peroxidation. This study provides mechanistic support for the traditional use of CME in ocular protection and underscores ferroptosis as a potential therapeutic target in ocular surface diseases.