Objective To compare the changes in biological indicators of human corneal epithelial (HCET) cells and rabbit corneas after exposure to different doses of ultraviolet B (UVB) radiation, so as to evaluate the impact of UVB radiation on corneal injury effects.

Methods In cell experiment, HCET cells were divided into groups with radiation doses of 0, 6, 12, 18, and 24 mJ/cm². The effect of UVB radiation on HCET cell viability was detected using the CCK-8 assay, and the level of intracellular DNA damage was assessed by immunofluorescence. In the animal experiment, 15 healthy New Zealand white rabbits (30 eyes) were randomly divided into groups with radiation doses of 0, 1.35, 2.16, 4.32, and 6.48 J/cm². The UVB exposure time for the radiation groups was 30 minutes per day for 3 consecutive days. Corneal injury was evaluated using methods such as slit-lamp microscopy, sodium fluorescein staining, central corneal thickness measurement, optical coherence tomography (OCT) imaging, and hematoxylin and eosin (HE) staining.

Results Compared with the control group, cell viability in the radiation groups gradually decreased, and the level of DNA damage gradually increased with increasing radiation dose. As the radiation dose increased in the radiation groups, the degree of corneal opacity in rabbits gradually worsened, the central corneal area gradually thickened, and OCT revealed high-intensity scattered light signals with the formation of shadow areas. Results from HE staining, immunohistochemistry, Western blot (WB), and sodium fluorescein staining showed that the 1.35 J/cm² group caused mild corneal injury, with damage reaching the corneal epithelial layer. In the 2.16 J/cm² group, the corneal injury presented as dense punctate distribution, with damage extending from the epithelial layer to the superficial stroma. The number of ephrin type-A receptor 2 (EphA2) protein-stained cells was relatively small, and the staining was light, showing a weak positive result. In the 4.32 J/cm² and 6.48 J/cm² groups, the corneal injury was irreversible, with damage gradually progressing from the corneal epithelial layer and superficial stroma to the endothelial layer. The number of EphA2 protein-stained cells was relatively large, and the staining was dark, showing a strong positive result.

Conclusion This study comprehensively evaluates the dose-dependent injury effects of UVB on HCET cells and New Zealand white rabbit corneas through cell and animal experiments. It elucidates that UVB radiation could induce corneal cell DNA damage, promote inflammatory responses, and trigger apoptosis by upregulating γ-phosphorylated histone H2AX (γH2AX) and EphA2. The self-repair ability and process of corneal injury are preliminarily explored, providing a basis for further research on mechanisms of corneal injury caused by ultraviolet radiation and the development of protective drugs.