ABSTRACT
Cerebral ischemia/reperfusion (I/R) injury refers to an aggravated brain tissue damage caused by the restoration of blood supply after acute ischemia for a period of time. Its pathogenesis is complex, including oxidative stress, inflammatory response, and excitatory amino acid toxicity. The effective clinical treatments of cerebral I/R injury after ischemic stroke (IS) are limited. Nuclear factor E 2-related factor 2 (Nrf2), the most critical antioxidant transcription factor in cells, can coordinate multiple cytoprotective factors to inhibit oxidative stress. Since Nrf2 signaling pathway is considered to be one of the most important cellular defense mechanisms against oxidative stress, targeting Nrf2 intervention has become an attractive therapeutic strategy in the prevention and treatment of cerebral I/R injury. This review focuses on the structure, regulation and function of Nrf2 signaling pathway, as well as its activation and potential therapeutic targets in cerebral I/R injury. The important role and future potential of Nrf2 pathway in the pathogenesis of cerebral I/R injury were discussed.