Ferroptosis is shown to promote osteoblast death and cause bone fracture in osteoporosis. This study aims to explore the role of naringenin in bone development and the underlying molecular mechanism. After treated with dexamethasone, cell proliferation was significantly inhibited in MC3T3-E1 cells. The levels of Fe²⁺ and ROS were increased when the level of GSH was decreased. The expression levels of GPX4 and SLC7A11, two markers of ferroptosis, were decreased. However, naringenin reduced the levels of Fe²⁺ and ROS when increased the expression levels of GPX4, SLC7A11, NRF2, HO-1, and Runx2. Furthermore, the ability of cell growth was restored. Conversely, knockdown of NRF2 counteracted the effects of naringenin. In addition, NRF2 was shown to be associated with TFAM based on the String database and knockdown of TFAM increased the levels of Fe²⁺ and ROS but decreased the level of GSH. Therefore, naringenin exhibited protective role against dexamethasone-induced ferroptosis in MC3T3-E1 cells by inhibiting NRF2 pathway.