Blue light induces corneal epithelial damage by activating the NLRP3 inflammasome pathway.

Blue light (BL) emitted from light-emitting diodes in digital devices poses significant risks to corneal health, by inducing oxidative stress and inflammation. This research elucidates the function of the NACHT, LRR and PYD domains-containing 3 (NLRP3) inflammasome in BL-induced corneal epithelial damage. In vivo, continuous BL exposure delayed corneal wound healing, shorten tear film break up time, and exacerbated epithelial defect areas in mice. In vitro, BL impaired the migration and viability of human corneal epithelial cells (HCECs) in a time- and intensity-dependent manner. Bioinformatic analysis identified NLRP3 as a predominant mediator, with BL upregulating the expression of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), Caspase-1, interleukin (IL)-1β, and IL-18 in both mouse corneas and HCECs. MCC950, the NLRP3 inhibitor, attenuated BL-induced cell death and oxidative stress, restoring the proliferative and migratory capacity of HCECs. In mice, application of topical MCC950 accelerated corneal epithelial wound healing, relived oxidative stress, and reduced ASC, and NLRP3 expression. These findings establish NLRP3 as a critical driver of BL-induced corneal damage and highlight the potential of NLRP3 pharmacological inhibition for mitigating BL-associated ocular surface disorders.