NIH Public Access HL Clifton BS J Yang PhD C…杨博士.pdfVIP

NIH Public Access Author Manuscript J Cardiovasc Pharmacol. Author manuscript; available in PMC 2013 July 01. N Published in final edited form as: I H J Cardiovasc Pharmacol. 2012 July ; 60(1): 70–75. doi:10.1097/FJC.0b013e3182580a5d. - P A A u Inhibition of soluble epoxide hydrolase limits niacin-induced t h o vasodilation in mice r M a 2 1 2 2 n A. B. Inceoglu, Ph.D. , H.L. Clifton, B.S. , J. Yang, Ph.D. , C. Hegedus, Ph.D. , B. D. u 2 1 s Hammock, Ph.D. , and S. Schaefer, M.D. c 1 r Department of Internal Medicine University of California Davis i p t 2Department of Entomology University of California Davis Abstract Background—The use of niacin in the treatment of dyslipidemias is limited by the common side effect of cutaneous vasodilation, commonly termed flushing. Flushing is thought to be due to N release of the vasodilatory prostanoids PGD and PGE from arachidonic acid metabolism through 2 2 I H the cyclooxygenase (COX) pathway. Arachidonic acid is also metabolized by the cytochrome - P P450 system which is regulated, in part, by the enzyme soluble epoxide hydrolase (sEH). A Methods: These experiments used an established murine model in which ear tissue perfusion was A measured by laser Doppler to test the hypothesis that inhibition of sEH would limit niacin-induced u