文摘
As one of the crucial factors of cataract formation, ultraviolet B (UVB) can lead to apoptosis of human lens epithelial cells. Zinc, a cell-protective metal against various toxic compounds, plays an important role in protecting target cells from damage. Nevertheless, it is still unclear whether zinc exhibits protective effect on human lens epithelial cells (HLE B-3) against UVB-induced damage. In this study, we investigated the protective effect of zinc chloride (ZnCl2) on UVB-induced HLE B-3 cell damage, explored the molecular mechanisms using real-time cell electronic sensing system, flow cytometry, real-time quantitative PCR and enzyme-linked immunosorbent assay techniques. The results show that ZnCl2 is a potential inhibitor of UVB-induced HLE B-3 cell damage, and the underlying mechanisms are involved in decreasing the overproduction of reactive oxygen species and mitochondrial dysfunction, promoting intracellular calcium homeostasis recovery, and thus maintaining cell normal physiological functions. Taken together, our findings suggest that appropriate zinc levels have potential for protecting HLE B-3 cells against UVB-induced damage, and this finding may be clinically useful.