Department of Pharmacology
Basic Science Building, Rm. 533
15 Dana Road
Valhalla, NY 10595
tel: (914) 594-4127/3117
1986 M.D. Shanghai 2nd Mil Medical University
1992 Ph.D. Beijing Institute of Basic Medical Sciences
Our current focus is on the mechanism of vitamin C in protecting the heart from heart failure. Our findings revealed that vitamin C stimulated the production of epoxyeicosatrienoic acids (EETs) and reduced levels of 20-hydroxyeicosatetraenoic acid (20-HETE) in Sprague-Dawley rats. Moreover, vitamin C can inhibit the expression of soluble epoxide hydrolase (sEH), the main enzyme responsible for EET metabolism. Thus, our results pointed out a unique mechanism of vitamin C in protecting the heart from heart failure through regulation of vasoactive lipid mediators, i.e. by preserving EETs and reducing 20-HETE. EETs are vasodilator, anti-inflammatory and antihypertensive lipid mediators, while 20-HETE is a vasoconstrictor, pro-inflammatory and pro-hypertensive lipid mediator produced by cytochrome P450 from arachidonic acid. The novel mechanism is consistent with reduced levels of EETs in cardiovascular diseases, the cardio-protective effects of EETs and a significant correlation of increased vitamin C with reduced incidences of heart failure. Our study suggested a prospect of combining vitamin C analogs with sEH inhibition for the prevention and treatment of heart failure.