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小米及小米多酚对高脂饮食诱导的大脑氧化应激的神经保护作用。

Neural Protective Effects of Millet and Millet Polyphenols on High-Fat Diet-Induced Oxidative Stress in the Brain.

机构信息

School of Medical Instrument and Food Engineering, University of Shanghai for Science and Technology, Jungong Road, Shanghai, 200093, China.

出版信息

Plant Foods Hum Nutr. 2020 Jun;75(2):208-214. doi: 10.1007/s11130-020-00802-6.

DOI:10.1007/s11130-020-00802-6
PMID:32078112
Abstract

A high fat diet (HFD) is considered to be a risk factor for the development of dementia because it increases oxidative stress in the brain; thus, diets rich in antioxidants, such as polyphenols, may protect against oxidative damage. In this study, we explored the antioxidant activity and neural protective function of millet on high fat diet-induced oxidative stress in rat brains. Our results suggested that the intake of millet could alleviate oxidative stress in the hippocampus and downregulate the expression of the Alzheimer's disease (AD)-related genes amyloid precursor protein (App), tau, and γ-secretase. Furthermore, we extracted millet polyphenols and verified whether they play important roles during this process. The results showed that millet polyphenols significantly prevented HO-induced cell death of SH-SY5Y cells and decreased oxidative stress levels in cells. In addition, the expression levels of pro-inflammatory factors and AD-related genes were also downregulated by treatment with millet polyphenols. The above results indicated that millet and millet polyphenols could exert neural protective effects under high fat diet-induced oxidative stress by upregulating the expression of antioxidant enzymes and downregulating the expression of AD-related genes.

摘要

高脂肪饮食(HFD)被认为是痴呆发展的一个风险因素,因为它会增加大脑中的氧化应激;因此,富含抗氧化剂的饮食,如多酚,可能有助于预防氧化损伤。在这项研究中,我们探索了小米对高脂肪饮食诱导的大鼠大脑氧化应激的抗氧化活性和神经保护作用。我们的结果表明,摄入小米可以减轻海马体的氧化应激,并下调阿尔茨海默病(AD)相关基因淀粉样前体蛋白(App)、tau 和 γ-分泌酶的表达。此外,我们提取了小米多酚,并验证了它们在这个过程中是否发挥重要作用。结果表明,小米多酚能显著防止 HO 诱导的 SH-SY5Y 细胞死亡,并降低细胞内的氧化应激水平。此外,用小米多酚处理还能下调促炎因子和 AD 相关基因的表达水平。上述结果表明,小米和小米多酚可以通过上调抗氧化酶的表达和下调 AD 相关基因的表达,在高脂肪饮食诱导的氧化应激下发挥神经保护作用。

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