Lutein Prevents High Fat Diet-Induced Atherosclerosis in ApoE-Deficient Mice by Inhibiting NADPH Oxidase and Increasing PPAR Expression
Lutein Prevents High Fat Diet-Induced Atherosclerosis in ApoE-Deficient Mice by Inhibiting NADPH Oxidase and Increasing PPAR Expression
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DOI：
10.1007/s11745-015-3992-1
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发表时间：
2015-03-01
期刊：
影响因子：
1.9
通讯作者：
Hao, Liping
中科院分区：
文献类型：
--
作者：
Han, Hao;Cui, Wei;Hao, Liping
流行病学和实验研究提供了支持性证据，表明叶黄素（一种主要的类胡萝卜素）可以作为动脉粥样硬化的化学预防剂，尽管其潜在的分子机制尚不清楚。本研究的主要目的是探讨叶黄素缓解动脉粥样硬化的作用及其参与氧化应激和脂质代谢的分子机制。雄性载脂蛋白 E 敲除小鼠 (n = 55) 被喂食正常食物或添加或不添加叶黄素的高脂肪饮食 (HFD)，持续 24 周。结果显示，高脂饮食会导致动脉粥样硬化形成、脂质代谢紊乱和氧化应激，但叶黄素治疗组观察到明显的改善。此外，补充叶黄素可逆转 HFD 刺激下主动脉血红素加氧酶 1 蛋白表达的降低，并增加主动脉烟酰胺腺嘌呤二核苷酸磷酸氧化酶的 mRNA 和蛋白表达。此外，在动脉粥样硬化小鼠中观察到的肝过氧化物酶体增殖物激活受体-a、肉碱棕榈酰转移酶1A、酰基辅酶A氧化酶1、低密度脂蛋白受体和B型清道夫受体I型mRNA和蛋白表达水平的降低在叶黄素治疗后显着增强。总而言之，这些数据增加了支持叶黄素抗动脉粥样硬化特性的新证据，并描述了其预防动脉粥样硬化的作用机制，包括氧化应激和脂质代谢的改善。
Epidemiological and experimental studies provide supportive evidence that lutein, a major carotenoid, may act as a chemopreventive agent against atherosclerosis, although the underlying molecular mechanisms are not well understood. The main aim of this study was to investigate the effects of lutein on the alleviation of atherosclerosis and its molecular mechanisms involved in oxidative stress and lipid metabolism. Male apolipoprotein E knockout mice (n = 55) were fed either a normal chow diet or a high fat diet (HFD) supplemented with or without lutein for 24 weeks. The results showed that a HFD induced atherosclerosis formation, lipid metabolism disorders and oxidative stress, but noticeable improvements were observed in the lutein treated group. Additionally, lutein supplementation reversed the decreased protein expression of aortic heme oxygenase-1 and increased the mRNA and protein expressions of aortic nicotinamide-adenine dinucleotide phosphate oxidase stimulated by a HFD. Furthermore, the decreased mRNA and protein expression levels of hepatic peroxisome proliferator-activated receptor-a, carnitine palmitoyltransferase 1A, acyl CoA oxidase 1, low density lipoprotein receptors and scavenger receptor class B type I observed in mice with atherosclerosis were markedly enhanced after treatment with lutein. Taken together, these data add new evidence supporting the anti-atherogenic properties of lutein and describing its mechanisms of action in atherosclerosis prevention, including oxidative stress and lipid metabolism improvements.