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γ-Aminobutyric Acid Attenuates High-Fat Diet-Induced Cerebral Oxidative Impairment via Enhanced Synthesis of Hippocampal Sulfatides
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2018-12-04 00:00:00 , DOI: 10.1021/acs.jafc.8b05246
Xu Si 1 , Yibo Li 1 , Yugang Jiang 2 , Wenting Shang 1 , Guanghou Shui 3 , Sin Man Lam 3 , Chris Blanchard 4 , Padraig Strappe 5 , Zhongkai Zhou 1, 4
Affiliation  

Long-term high-fat diet (HFD) in rats triggered cerebral oxidative stress, reflected by reactive oxygen species accumulation and antioxidant decline in peripheral and cerebral tissues, together with hippocampal lipid disturbance, particularly for triglyceride accumulation and sulfatide deficiency. Hippocampal formation and cerebral cortex also exhibited pathological changes, characterized by neurofibrillary tangle and reduced Nissl bodies. Sulfatides were noted to protect hippocampal neurons from oxidative damage through the clearance of β-amyloid protein, with apolipoprotein E transporting and low-density lipoprotein receptor binding. Delightedly, we found γ-aminobutyric acid (GABA) supplement delivered by rice bran to rats significantly promoted hippocampal sulfatide synthesis and reversed the HFD-induced sulfatide deficiency and oxidative-triggered cerebral impairment. Elevated GABA concentration in hippocampus and the activation of GABA B-type receptors might be the primary contributors. This study demonstrated the potential of GABA-enriched rice bran as a novel dietary supplement to enhance a sulfatide-based therapeutic approach for neurodegenerative diseases in the early stages.

中文翻译:

γ-氨基丁酸通过增强海马硫酯的合成来减轻高脂饮食诱导的脑氧化损伤

大鼠的长期高脂饮食(HFD)触发了脑部氧化应激反应,反映在周围和大脑组织中活性氧的积累和抗氧化剂的下降,以及海马脂质紊乱,特别是甘油三酸酯累积和硫脂缺乏症。海马形成和大脑皮层也表现出病理变化,其特征是神经原纤维缠结和尼氏体减少。硫酸盐被认为可以通过清除β-淀粉样蛋白,载脂蛋白E转运和低密度脂蛋白受体结合来保护海马神经元免受氧化损伤。很高兴 我们发现米糠向大鼠输送的γ-氨基丁酸(GABA)补充剂可显着促进海马硫酸盐合成,并逆转HFD诱导的硫酸盐缺乏和氧化触发的脑损伤。海马中GABA浓度升高和GABA B型受体的激活可能是主要的促成因素。这项研究证明了富含GABA的米糠作为新型膳食补充剂的潜力,可以在早期阶段增强基于硫酸盐的神经退行性疾病的治疗方法。
更新日期:2018-12-04
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