| Literature DB >> 31698143 |
Jogen Atone1, Karen Wagner1, Kenji Hashimoto2, Bruce D Hammock3.
Abstract
Cytochrome P450 (CYP) metabolism of arachidonic acid (ARA) produces epoxy fatty acids (EpFAs) such as epoxyeicosatrienoic acids (EETs) that are known to exert protective effects in inflammatory disorders. Endogenous EpFAs are further metabolized into corresponding diols by the soluble epoxide hydrolase (sEH). Through inhibition of sEH, many studies have demonstrated the cardioprotective and renoprotective effects of EpFAs; however, the role of sEH inhibition in modulating the pathogenesis of neuroinflammatory disorders is less well described. In this review, we discuss the current knowledge surrounding the effects of sEH inhibition and EpFA action in neuroinflammatory disorders such as Parkinson's Disease (PD), stroke, depression, epilepsy, and Alzheimer's Disease (AD), as well as the potential mechanisms that underlie the therapeutic effects of sEH inhibition.Entities:
Keywords: Alzheimer’s disease (AD); Depression; Epoxyeicosatrienoic acid (EET); Neuroinflammation; Parkinson’s disease (PD); Soluble epoxide hydrolase (sEH); Stroke
Mesh:
Substances:
Year: 2019 PMID: 31698143 PMCID: PMC7067627 DOI: 10.1016/j.prostaglandins.2019.106385
Source DB: PubMed Journal: Prostaglandins Other Lipid Mediat ISSN: 1098-8823 Impact factor: 3.072