Reduction of oxidative stress and apoptosis in hyperlipidemic rabbits by ellagic acid

被引:91
|
作者
Yu, YM [1 ]
Chang, WC
Wu, CH
Chiang, SY
机构
[1] China Med Univ, Dept Nutr, Taichung 40402, Taiwan
[2] China Med Univ, Dept Sports Med, Taichung 40402, Taiwan
[3] China Med Univ, Dept Biol Sci & Technol, Taichung 40402, Taiwan
[4] China Med Univ, Dept Pharmacol, Taichung 40402, Taiwan
[5] China Med Univ, Inst Chinese Med Sci, Taichung 40402, Taiwan
来源
JOURNAL OF NUTRITIONAL BIOCHEMISTRY | 2005年 / 16卷 / 11期
关键词
antioxidant; ellagic acid; oxidative stress; 8-(OH)dG; apoptosis; atherosclerosis;
D O I
10.1016/j.jnutbio.2005.03.013
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Oxidative stress is one of the major risk factors for coronary artery disease. Ellagic acid is a phenolic compound present in fruits and nuts, and has been found to have antioxidative property. Twenty-four New Zealand white (NZW) rabbits were assigned randomly into four dietary groups. The normal group was fed regular rabbit chow, and the cholesterol group was fed a high fat and cholesterol diet. The ellagic acid (E) group and probucol group were fed the same diet as the cholesterol group plug the addition of 1% (w/w diet) ellagic acid and probucol, respectively. Oxidative stress [as measured by plasma lipids, oxygen free radicals and thiobarbituric acid reactive substances (TBARS)] increased in the cholesterol group compared with the normal group; however, it decreased in the probucol and E groups compared with the cholesterol group. Forty-five percent of the intimal surface of the thoracic aorta was covered with atherosclerotic lesions in the cholesterol group, but only 2-3% was covered in the E and probucol groups. The aortic level of 8-(OH)dG and the expression of caspase-8, caspase-9 and Fas ligand were also suppressed after ellagic acid supplement. These results indicated that ellagic acid could prevent atherosclerosis via suppression of oxidative stress and apoptosis in hyperlipidemic rabbits. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:675 / 681
页数:7
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