Abstract
Purpose:
We evaluated the capacity of rebamipide (REB) to alleviate corneal epithelial damage induced via blue light (BL) exposure.
Methods:
Eight-week-old C57BL/6 mice were exposed to BL (410 nm, 100 J) twice daily for 10 days. The mice were randomly divided into 5 groups: 1 untreated and 4 groups receiving BL exposure ± different topical treatments: BL exposure alone, carboxymethylcellulose, 5% N-acetylcysteine, and REB. Reactive oxygen species (ROS) levels were assessed, and Bcl-2-associated X protein (BAX) protein was analyzed. Apoptotic cells were detected, inflammatory cytokine levels [tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6)] were measured using enzyme-linked immunosorbent assay (ELISA), and histopathological changes in the cornea were evaluated using hematoxylin and eosin (H&E) staining.
Results:
The REB group demonstrated significantly lower BL exposure-induced ROS levels (P < 0.01) and BAX expression (P < 0.01) than the BL group. The number of Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) positive cells were lower in the REB group than in the BL group (P < 0.01). Furthermore, ELISA analysis revealed significantly reduced TNF-α and IL-6 levels in the REB group relative to BL group levels (P < 0.01). Hematoxylin and eosin staining showed preservation of corneal epithelial thickness.
Conclusions:
Rebamipide alleviated BL-induced oxidative damage to ocular surfaces by reducing ROS levels, inhibiting apoptosis, and suppressing inflammatory cytokine expression.
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