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. Author manuscript; available in PMC: 2017 Sep 13.
Published in final edited form as: CNS Neurol Disord Drug Targets. 2017;16(3):326–338. doi: 10.2174/1871527316666170102120211

Fig 1.

Fig 1

Mechanisms of select dietary Nrf2 activators. (A) Under physiological or baseline conditions, Nrf2 is sequestered by Keap1, leading to its ubiquitination and degradation by the proteasome. (B) Two mechanisms are involved in Nrf2 activation. The first is by modification of the cysteines in Keap1, which leads to conformational changes in this protein and the subsequent release of Nrf2. The second mechanism is by activation of kinases that phosphorylate Nrf2 and thereby free it from Keap1-mediated sequestration. After nuclear translocation, Nrf2 binds to the antioxidant response element (ARE) in the promoter regions of phase 2 enzyme genes. SFN, curcumin, and OSC all activate Nrf2 by the first mechanism, whereas RES and capsaicin function through the second mechanism and EGC and lycopene work through both mechanisms. Keap1: Kelch like ECH associated protein 1; SFN: sulforaphane; EGCG: epigallocatechin gallate; OSC: organosulfur compound; RES: resveratrol.