The protective mechanism of Grx2 in ultraviolet-B (UVB)-induced cataract formation

We established a mouse cataract model by irradiating Grx2 knockout (KO) and knock-in (KI) genetically modified mice with UVB to explore the protective mechanism of Grx2 against UVB lens damage.

After irradiating Grx2 KO and Grx2 KI mice with UVB lamps, we observed and recorded the general physiological conditions and lens opacity of the mice. The crystalline grading system of the University of Oxford was used to classify the opacity of the lens. Lens reactive oxygen species (ROS) contents were detected using a microplate reader, western blot, and enzyme-linked immunosorbent assay (ELISA) to detect antioxidant and antioxidant enzyme contents. Statistical analysis of the recorded data was performed by using SPSS 19.0 software.

After UVB irradiation, the weight of Grx2 KO mice was slightly lower than that of wild-type (WT) mice of the same age. Compared to WT mice, the lens opacity of Grx2 KO mice appeared earlier, the nucleus density of the lens increased, and the opacity increased in the first week after UVB irradiation. Meanwhile, the lenses of Grx2 KI mice remained transparent. The experiment showed that the content of ROS increased, the level of glutathione (GSH) decreased, the content of 8-OHdG increased, and the expression of BCL2 decreased after UVB irradiation. Compared to WT mice, these changes were more significant in Grx2 KO mice.

This experiment found that knocking out the Grx2 gene accelerated the occurrence and development of UVB-induced cataracts in mice and that Grx2 plays an important role in the oxidative damage caused by UVB radiation by repairing the antioxidant enzymes of the lens. This study provides a new animal model and research ideas for the study of cataract pathogenesis.