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Proposed mechanism of the role of sEH in depression. Inflammation or stress can increase the expression of sEH in the brain, resulting in enhanced metabolism of anti-inflammatory PUFA epoxides (EpFAs). Subsequently, increased expression of sEH can decrease BDNF-TrkB signaling and synaptogenesis, leading to depressive symptoms. The sEH inhibitors may have antidepressant actions in depressed patients. (modified from Hashimoto, 2016).
