Neuroinflammation is a physiologic response aimed at protecting the central nervous system during injury. However, unresolved and chronic neuroinflammation can lead to long term damage and eventually neurologic disease including Parkinson's disease, Alzheimer's disease and dementia. Recently, enhancing the concentration of epoxyeicosatrienoic acids (EETs) through blocking their hydrolytic degradation by soluble epoxide hydrolase (sEH) has been applied towards reducing the long-term damage associated with central neurologic insults. Evidence suggests this protective effect is mediated, at least in part, through polarization of microglia to an anti-inflammatory phenotype that blocks the inflammatory actions of prostaglandins and promotes wound repair. This mini-review overviews the epidemiologic basis for using sEH inhibition towards neuroinflammatory disease and pharmacologic studies testing sEH inhibition in several neurologic diseases. Additionally, the combination of sEH inhibition with other eicosanoid signaling pathways is considered as an enhanced approach for developing potent neuroprotectants.

神经炎症是一种生理反应，旨在保护受伤期间的中枢神经系统。但是，未解决的慢性神经炎症会导致长期损害，并最终导致神经系统疾病，包括帕金森氏病，阿尔茨海默氏病和痴呆症。近来，通过阻止环氧二十碳三烯酸（EET）被可溶性环氧化物水解酶（sEH）水解降解来提高其浓度已被用于减少与中枢神经损伤相关的长期损害。有证据表明，这种保护作用至少部分地通过小胶质细胞的极化转变为一种抗炎表型，该表型阻断了前列腺素的炎性作用并促进了伤口的修复。这份小型综述概述了使用sEH抑制作用治疗神经炎性疾病的流行病学基础，以及在几种神经系统疾病中测试sEH抑制作用的药理研究。另外，sEH抑制与其他类花生酸信号通路的组合被认为是开发有效神经保护剂的一种增强方法。