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Nutrition and Disease

An Anthocyanin-Rich Extract from Black Rice Enhances Atherosclerotic Plaque Stabilization in Apolipoprotein E–Deficient Mice¹

Department of Nutrition, School of Public Health, Sun Yat-sen University (Northern Campus), Guangzhou 510080, P. R. China

^* To whom correspondence should be addressed. E-mail: lingwh{at}mail.sysu.edu.cn.

Black rice and its pigment fraction may have antiatherogenic activity, but the exact component contributing to the beneficial effect remains unclear. The aim of the present study was to investigate the influence of the anthocyanin-rich extract from black rice on the vulnerability of advanced plaques in apolipoprotein (apo) E-deficient mice. Using LC-MS, the anthocyanin-rich extract from black rice was identified as containing cyanidin-3-glucoside and peonidin-3-glucoside. ApoE-deficient mice (n = 30; 30 wk old) were randomly divided into 3 groups: a control group (fed the AIN-93G diet), the simvastin group [simva; fed the AIN-93G diet containing simvastatin, 50 mg/(kg·d)], or the anthocyanin-rich extract group [antho; fed the AIN-93G diet supplemented with anthocyanin-rich extract from black rice, 300 mg/(kg·d)]. After 20 wk of intervention, the plaque area that developed in the brachiocephalic artery of mice in the antho group was smaller than that of the control mice. Both the antho and simva groups had lower frequencies of the large necrotic core and thin fibrous cap in plaques than the control group. Collagen I was increased and matrix metalloproteinase-1 contents were reduced in the brachiocephalic lesion of both the antho and simva groups compared with the control group. Furthermore, mRNA levels of tissue factor and inducible nitric oxide synthase in aortae were decreased in the antho and simva groups. Supplementation of anthocyanin-rich extract improved the lipid profile by decreasing serum triglyceride, total cholesterol, and non-HDL cholesterol. These results suggest that chronic diet intake of anthocyanin-rich extract from black rice may enhance plaque stabilization in old apoE-deficient mice. The underlying mechanism is related mainly to inhibiting proinflammatory factors and improving the serum lipid profile.

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