Zinc chloride inhibits human lens epithelial cell migration and proliferation involved in TGF-β1 and TNF-α signaling pathways in HLE B-3 cells.

Zinc is one of the most abundant essential elements in the human body, which is an essential, coenzyme-like component of many enzymes, and is indispensable to their functions. However, high levels of zinc ions can lead to cell damage. In the present study, we explored the effects of high concentrations of zinc chloride (ZnCl2) on lens epithelial cell proliferation and migration and further investigated the effects of different concentrations of ZnCl2 on caspase-9 and caspase-12, transforming growth factor-beta 1 (TGF-β1), and tumor necrosis factor-alpha (TNF-α). We found that ZnCl2 could inhibit human lens epithelial (HLE) B-3 cell migration and induce apoptosis/necrosis. In addition, ZnCl2 can efficiently decrease the expressions of caspase-9 and caspase-12, increase the expression of TNF-α at both gene and protein levels, and thus induces cell death. Taken together, our results indicate that ZnCl2 can inhibit HLE B-3 cell migration and proliferation by decreasing the expression of TGF-β1 and increasing the expression of TNF-α and finally lead to HLE B-3 cell death.