Echinatin mitigates H2O2-induced oxidative damage and apoptosis in lens epithelial cells via the Nrf2/HO-1 pathway

Background. Oxidative stress has been reported to be an early factor in the development of cataracts. Echinatin (Ech) is an active ingredient of licorice that exhibits antioxidant effects. Objectives. To investigate the effects of Ech on oxidative stress-induced lens epithelial cell (LEC) damage. Materials and methods. Human lens epithelial B3 cells (HLECs) were exposed to hydrogen peroxide (H2O2) and were pretreated with or without Ech. For rescue experiments, ML385, an inhibitor of the Nrf2 pathway, was added into the medium. Results. Echinatin reversed the H(2)O(2)induced reduction of cell viability in B3 cells. Additionally, H2O2 induced oxidative stress, evidenced by an increase of reactive oxygen species (ROS) and malondialdehyde (MDA) levels, and a decrease in superoxide dismutase (SOD) and catalase (CAT) levels, which could be abolished by Ech. Echinatin treatment also reduced HLEC apoptosis induced by H2O2. In addition, Ech pretreatment promoted Bcl-2 expression, and suppressed Bax and caspase-3 expression levels, in H2O2-treated B3 cells. Moreover, H2O2 significantly reduced Nrf2 nuclear localization, as well asHO-1 and NQO1 expression, which could be reversed by Ech. Inhibition of Nrf2 by ML385 aggravated H2O2-induced oxidative damage and apoptosis in HLECs, and the protective effects of Ech on H2O2-induced oxidative damage and apoptosis could be restored by ML385. Conclusions. Echinatin mitigates H2O2-induced oxidative damage and apoptosis in HLECs via the Nrf2/HO-1 pathway, suggesting that Ech may be a potential drug for the treatment of cataracts.

Automated summary

Echinatin can alleviate oxidative damage and apoptosis induced by H2O2 in HLECs through the Nrf2/HO-1 pathway, indicating that Ech may be a potential drug for the treatment of cataracts.