|Nie, Lin - TUFTS/HNRCA|
|Meydani, Mohsen - TUFTS/HNRCA|
Submitted to: Atherosclerosis
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 18, 2005
Publication Date: June 1, 2006
Citation: Nie, L., Wise, M.L., Peterson, D.W., Meydani, M. 2006. Avenanthramide, a polyphenol from oats, inhibits vascular smooth muscle cell proliferation and enhances nitric oxide production. Atherosclerosis. 186(2):260-6. Interpretive Summary: Proliferation of vascular smooth muscle cells and impaired production of nitric oxide by endothelial (living cells) and vascular (blood vessel) smooth muscle cells contribute to the development of heart disease. We investigated the effects of avenanthramide, a unique antioxidant from oats, on these processes in cultured cells. We found that the avenanthramide inhibited vascular smooth muscle cell proliferation in a dose-dependent manner and it also enhanced nitric oxide production by vascular smooth muscle cells and by human aortic endothelial cells. These results suggest that avenanthramide from oats may contribute to the prevention of heart disease through its effects on these processes. This is in addition to the well-known effects of oats on cholesterol lowering. This research could lead to a significant impact for the value of oats in a heart-healthy diet.
Technical Abstract: The proliferation of intimal vascular SMC and impaired NO production are both crucial pathophysiological processes in the initiation and development of atherosclerosis. Epidemiological data have indicated that diet rich in whole grain foods is associated with reduced risk of developing atherosclerosis and hypertension. Earlier we have shown that avenanthramides, polyphenols found exclusively in oat grain, inhibited pro-inflammatory cytokines and adhesive interaction of immune and endothelial cells. Here we report the effect of specific avenanthramide C (Av-C) prepared synthetically on human aortic SMC (HASMC) proliferation and NO production. We found that Av-C dose-dependently inhibited serum-induced HASMC proliferation as measured by [3H] thymidine incorporation and counting the cell number. The IC 50 of Av-C was around 50 microM. Incubation of cells with 120 microM Av-C for 4 days inhibited cell growth by more than 50 per cent This inhibitory effect of Av-C was associated with an increase in the expression of p21CIP1 and a decrease in the phosphorylation of pRB. In addition, Av-C treatment significantly increased the NO production and eNOS mRNA expression as measured by real time PCR. At 80 microM, the NO production and eNOS mRNA expression levels increased by 2.1 and 3.5 fold, respectively. The HASMC expression of vascular cell adhesion molecular-1 (VCAM-1) was not affected by Av-C treatment. These data suggest that the avenanthramides in oats may have great potential to prevent vascular dysfunction and development of atherosclerotic lesion by inhibiting vascular SMC proliferation and increasing NO production. Supported by USDA agreement No.58-1950-9-001.