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Emerging evidence has shown that four\u2010octyl itaconate (OI) activates Nrf2 cascade. In this study, the chondroprotective effects of OI on H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>\u2010stimulated chondrocytes and DMM\u2010induced osteoarthritis (OA) progression were investigated. In primary murine chondrocytes, OI interrupted the binding of Keap1 and Nrf2, leading to accumulation and nuclear translocation of Nrf2 protein, as well as transcription and expression of Nrf2\u2010dependent genes, such as <jats:italic>HO-1<\/jats:italic>, <jats:italic>NQO1<\/jats:italic>, and <jats:italic>GCLC<\/jats:italic>. Furthermore, OI inhibited cell death and apoptosis, as well as H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>\u2010stimulated ROS generation, lipid peroxidation, superoxide accumulation, and mitochondrial depolarization in chondrocytes, which were abolished by the silence or depletion of Nrf2. In addition, <jats:italic>in vivo<\/jats:italic> experiments revealed the therapeutic effects of OI on OA progression in a DMM mouse model. 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