Effects and mechanism of peroxiredoxin-6 on ultraviolet-induced corneal injury in rats

To investigate the therapeutic effect of peroxiredoxin-6(PRDX6)on ultraviolet-induced corneal injury in rats and explore the mechanism, a rat model of corneal injury was established by exposing to ultraviolet. Male Wister rats were randomly divided into control group, dexamethasone(DXM)group and PRDX6 group. All the rats were administered four times a day and for 12 days. The corneal opacity was observed with a slit-lamp microscope. Histopathologic changes were observed with light microscope. The content of corneal malonaldehyde(MDA)was determined by thiobarbituric acid test; the total antioxidative capacity(TAOC)was detected by chemical colorimetric test. P38 MAPK signaling pathway was detected with the method of Western blot and gene expression of cytokines was measured by RT-PCR. Compared with the control group, PRDX6 treatment significantly reduced corneal opacity, improved corneal pathology injury, decreased the MDA content and increased the TAOC. In the PRDX6 group, the level of phosphorylated p38 protein was significantly lower than that in the control group. The gene expression of cytokine was different between the control and PRDX6 groups(P < 0. 05). PRDX6 showed therapeutic effect in the rat model of ultraviolet-induced corneal injury, which may be because it could alleviate the oxidative damage, suppress p38 MAPK phosphorylation and regulate the gene expression of cytokine.