The current study was aimed at evaluating the therapeutic implication of apigenin and to elucidate the underlying mechanism. The -butyl hydroperoxide (-BHP) at 200 M was used to induce oxidative stress-associated injury in ARPE-19 cells. Apigenin at concentrations less than 800 M did not cause cytotoxic effects on ARPE-19 cells. Cell viability assay showed that apigenin at 200 M significantly promoted cell survival in -BHP-treated ARPE-19 cells. Additionally， apigenin at 100 M significantly protected ARPE-19 cells from -BHP-induced apoptosis. Molecular examinations demonstrated that apigenin at 400 M significantly upregulated the mRNA and protein expression of Nrf2 and stimulated its nuclear translocation in ARPE-19 cells treated with or without -BHP. Apigenin 400 M also significantly elevated the expression of HO-1， NQO1， and GCLM at both mRNA and protein levels in the presence or absence of -BHP. Furthermore， apigenin at 400 M significantly increased the activities of SOD， CAT， GSH-PX， and T-AOC and reduced the levels of ROS and MDA in -BHP-treated ARPE-19 cells. However， these effects of apigenin were all abolished by being transfected with Nrf2 siRNA. Collectively， our current data indicated that apigenin exerted potent antioxidant properties in ARPE-19 cells challenged with -BHP， which were dependent on activation of Nrf2 signaling.