| Abstract
| - Aims:. Ultraviolet B (UVB) irradiation activates nuclear factor-kappa B (NF-κB) and cyclo-oxygenase (COX). The COX inhibitors are protective against UVB-induced skin damage. The aim of this study is to determine the effect of lornoxicam, a potent COX inhibitor, on UVB-induced corneal damage and its mechanism in a mouse model. Methods:. Eighty female ICR mice were randomly divided into four groups. Corneal damage was graded based on the degree of haze. NF-κB activation in the cornea was examined using an electrophoretic mobility shift assay, and tumour necrosis factor (TNF)-α production was determined by enzyme-linked immunosorbant assay (ELISA) 6, 24 and 72 h after irradiation. The histopathological changes in cornea were examined under the transmission electronic microscope at 24 h up to 7 days following irradiation. Results:. UVB irradiation (1.2 J/cm2) induced a significant and sustained increase in the NF-κB-DNA binding activity and TNF-α production in the cornea, with the peak at 24 h. Apparent stromal oedema and corneal opacity as well as severe histopathological damage including epithelial exfoliation, keratocyte loss and endothelial oedema were observed after irradiation. Treatment with lornoxicam (0.4 mg/kg, intraperitoneal) significantly lowered the grade of corneal opacity and remarkably ameliorated the ultrastructural damage induced by irradiation. Lornoxicam treatment significantly suppressed UVB-induced increases in NF-κB-DNA binding and TNF-α expression. Conclusion:. Lornoxicam treatment attenuates UVB-induced corneal damage via inhibition of NF-κB activation.
|
