Abstract
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. To investigate the effects of Ech on oxidative stress-induced lens epithelial cell (LEC) damage. 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. Echinatin reversed the H2O2-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 as HO-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. 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.
Highlights
Oxidative stress has been reported to be an early factor in the development of cataracts
Inhibition of Nrf[2] by ML385 aggravated H2O2-induced oxidative damage and apoptosis in Human lens epithelial B3 cells (HLECs), and the protective effects of Ech on H2O2-induced oxidative damage and apoptosis could be restored by ML385
Echinatin mitigates H2O2-induced oxidative damage and apoptosis in HLECs via the Nrf2/heme oxygenase 1 (HO-1) pathway, suggesting that Ech may be a potential drug for the treatment of cataracts
Summary
Oxidative stress has been reported to be an early factor in the development of cataracts. Studies have shown that the protein and gene expression of Nrf[2] in the lens significantly decreases with age.[11,12] The decreased activity of Nrf[2] limits the transcription of its downstream antioxidant enzymes and causes the antioxidant system to fail, which leads to age-related cataracts.[12] Targeted activation of Nrf[2] signaling can protect LECs from damage induced by oxidative stress.[13,14]
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