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Cytochrome P450 derived epoxidized fatty acids as a therapeutic tool against neuroinflammatory diseases.
ProstaglandIns & Other Lipid Mediators ( IF 2.5 ) Pub Date : 2019-11-05 , DOI: 10.1016/j.prostaglandins.2019.106385
Jogen Atone 1 , Karen Wagner 1 , Kenji Hashimoto 2 , Bruce D Hammock 1
Affiliation  

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.

中文翻译:

细胞色素 P450 衍生的环氧化脂肪酸作为神经炎症性疾病的治疗工具。

花生四烯酸 (ARA) 的细胞色素 P450 (CYP) 代谢产生环氧脂肪酸 (EpFA),例如环氧二十碳三烯酸 (EET),已知它们在炎症性疾病中发挥保护作用。内源性 EpFA 通过可溶性环氧化物水解酶 (sEH) 进一步代谢成相应的二醇。通过抑制 sEH,许多研究已经证明 EpFA 具有心脏保护和肾脏保护作用;然而,sEH 抑制在调节神经炎症性疾病发病机制中的作用尚不清楚。在这篇综述中,我们讨论了关于 sEH 抑制和 EpFA 作用在帕金森病 (PD)、中风、抑郁症、癫痫和阿尔茨海默病 (AD) 等神经炎症性疾病中的作用的当前知识,以及其潜在机制sEH 抑制的治疗效果。
更新日期:2019-11-01
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