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. 2022 Apr 5;35(2):e100700. doi: 10.1136/gpsych-2021-100700

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© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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Biological mechanisms of sulforaphane. ARE, antioxidant response element; ERK, extracellular signal-regulated kinase; GCL, glutamate cysteine ligase; HO1, haem oxygenase 1; IκB, inhibitor of NF-κB; JNK, c-Jun N-terminal kinase; Keap1, Kelch-like ECH-associated protein 1; MAPK, mitogen-activated protein kinase; NF-κB, nuclear factor-κB; NQO1, NAD(P)H quinone dehydrogenase 1; Nrf2, nuclear factor erythroid 2-related factor 2.