Supplementation of the black rice outer layer fraction to rabbits decreases atherosclerotic plaque formation and increases antioxidant status.
The influence of the supplementation of black and white rice outer layer fractions on atherosclerotic plaque formation induced by hypercholesterolemia was investigated in rabbits. Male rabbits (n = 32) were randomly divided into four groups. They were fed nonpurified diet (normal group), a lard (3.5 g/100 g) with high cholesterol (0.5 g/100 g) diet (HC group); the HC diet with 5 g/100 g white rice outer layer fraction (WRF group); or the HC diet with 5 g/100 g black rice outer layer fraction (BRF) for 2 mo. Blood samples were collected for determination of lipid concentration and oxidative and antioxidative status variables, and aortae were taken for the assessment of atherosclerotic plaques. The atherosclerotic plaque area in rabbits fed the BRF diet was 66% lower than that of the HC or WRF rabbits (P < 0.001). Supplementation of the black rice outer layer significantly (P < 0.05) lowered aortic 8-hydroxy-2'-deoxyguanosine (8-OHdG) (-52%, -44%) compared with the WRF or HC diets (P < 0.05). There were no differences in aortic 8-OHdG levels between rabbits fed the BRF and normal diets. The BRF diet significantly (P < 0.05) decreased the malondialdehyde (MDA) level of serum (-37%) and aortic artery (-50%) compared with the WRF diet. There were no differences in the concentrations of serum total cholesterol (TC), LDL cholesterol (LDL-C), HDL-C or the ratio of apoprotein (apo)I/apoB among the HC, WRF and BRF groups. Similarly, there were no differences in the serum vitamin E concentration and erythrocyte and aorta superoxide dismutase (SOD) activities among rabbits fed these diets. The serum concentration of most fatty acids except 18:1 did not differ between the WRF and the BRF groups. We conclude that the inhibition of atherosclerotic plaque formation derived from the black rice outer layer fraction in rabbits might be mediated by antioxidative or anti-inflammatory effects.
Ling
Wen Hua
WH
Department of Clinical Nutrition, Sun Yat-sen University of Medical Sciences, Guangzhou, 510080, PR-China. whling@gzsums.edu.cn
Wang
Lin Llin
LL
Ma
Jing
J
D000080242:8-Hydroxy-2'-Deoxyguanosine; D000704:Analysis of Variance; D000818:Animals; D001011:Aorta / Q000473:pathology*; D001161:Arteriosclerosis / Q000139:chemically induced / Q000517:prevention & control*; D002791:Cholesterol, Dietary / Q000009:adverse effects*; D003849:Deoxyguanosine / Q000031:analogs & derivatives* / Q000097:blood; D005227:Fatty Acids / Q000097:blood; D006937:Hypercholesterolemia / Q000139:chemically induced / Q000503:physiopathology; D008055:Lipids / Q000097:blood*; D008099:Liver / Q000378:metabolism*; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D012275:Oryza; D010084:Oxidation-Reduction; D011817:Rabbits; D011897:Random Allocation; D013482:Superoxide Dismutase / Q000378:metabolism; D014810:Vitamin E / Q000097:blood
D002791:Cholesterol, Dietary; D005227:Fatty Acids; D008055:Lipids; D014810:Vitamin E; D008315:Malondialdehyde; D000080242:8-Hydroxy-2'-Deoxyguanosine; D013482:Superoxide Dismutase; D003849:Deoxyguanosine