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. 2022 Jun 16;13:927898. doi: 10.3389/fphar.2022.927898

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Copyright © 2022 Park, Noh, Jung, Leem, Hyun, Chang, Kwon, Kim, Lee and Choi.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Graphical description of fisetin suppressing H₂O₂-induced oxidative damage in human RPE ARPE-19 cells through Nrf2-mediated HO-1 activation. In brief, fisetin significantly enhanced the expression of HO-1 along with activation of Nrf2 and reduced DNA damage, mitochondrial dysfunction and apoptosis in H₂O₂-treated ARPE-19 cells. However, these beneficial effects were abolished in the presence of an inhibitor of HO-1 activity, indicating that the enhanced expression of HO-1 contributed to the mitigating effect of fisetin on oxidative stress-induced cellular injury. Taking together, these results provide strong evidence that fisetin as a ROS scavenger can rescue RPE cells from oxidative damage through activation of the Nrf2/HO-1 axis.