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Soluble Epoxide Hydrolase Is Involved in Angiotensin II‐induced Atherosclerosis

Angiotensin II may contribute to the development and progression of atherosclerotic lesions because of its growth and proinflammatory effects. Epoxyeicosatrienoic acids(EETs), hydrolyzed and degraded by soluble epoxide hydrolase (sEH), enhance arteries dilation and provide anti‐inflammation, thus are cardioprotective. In this study, we investigated the role of sEH in angiotensin II (Ang II)‐induced atherosclerosis in apoE‐deficient mice. AngII (1.44 mg/kg·d) was administered to apoE‐deficient mice via osmotic minipumps. The animals were placed on either standard chow or an atherogenic diet with or without sEH‐selective inhibitors. After 4‐week atherogenic diet, the mean atherosclerotic lesion area in ventricle efferent track of animals was increased compared to those on a standard chow diet. AngII treatment increased the lesion area, which was further increased by atherogenic diet. On the other hand, sEH‐inhibitor significantly reduced atherogenesis. Western blot shows that AngII increased the expression of sEH and ICAM‐1 in mouse aortas. Furthermore, sEH inhibitor abolished the ICAM‐1 induction by AngII. Our results suggest that sEH is upregulated by Ang II, which is atherogenic.