The soluble epoxide hydrolase (sEH) is involved in the metabolism of arachidonic, linoleic, and other fatty acid epoxides, endogenous chemical mediators that play an important role in blood pressure regulation and inflammation. AUDA is a potent sEH inhibitor with IC50s of 18±1 and 69±2 nM for the mouse and human sEH, respectively[1]. AUDA (0.3 to 10 μg/mL) dose-dependently suppressed the proliferation of rat VSMCs (vascular smooth muscle cells) exposed to PDGF (platelet-derived growth factor) for 48 h. AUDA (1–30 μg/mL) dose-dependently inhibited the protein expression of Pin1 and increased HO-1 (heme oxygenase-1) protein levels in PDGF-treated VSMCs at a dose of 3 μg/mL, although potent induction was seen only at 30 μg/mL. PDGF increased COX-2 protein levels in rat VSMCs, and AUDA (1–30 μg/mL; 30 min) dose-dependently upregulated COX-2 expression[2]. Furthermore, in the mouse model of Kawasaki disease (KD), AUDA reduced the protein expression of MMP-9, IL-1β and TNF-α, indicating that AUDA may alleviate inflammatory reactions in the coronary arteries of KD model mice[3].
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