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首页> 外文期刊>The Journal of Nutritional Biochemistry >Green tea catechins prevent cognitive deficits caused by A beta1-40 in rats.
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Green tea catechins prevent cognitive deficits caused by A beta1-40 in rats.

机译：绿茶儿茶素可预防大鼠Aβ1-40引起的认知缺陷。

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Amyloid beta peptide (A beta)-induced oxidative stress is involved in the pathogenesis of Alzheimer's disease (AD). In contrast, green tea catechins confer potent antioxidative defense to brain neurons. Therefore, we examined whether long-term administration of green tea catechins [Polyphenon E (PE): 63% of epigallocatechin-3-gallate, 11% of epicatechin, 6% of (-)-epigallocatechin and 6% of (-)-epicatechin-gallate] prevents cognitive impairment in an animal model of AD, rats infused with A beta1-40 into the cerebral ventricle. Five-week-old male Wistar rats fed with an MF diet were randomly divided into two groups: 0.0% PE (rats administered with water only) and 0.5% PE (rats administered with 5 g/L of PE). Twenty weeks after the PE administration, the 0.0% PE group was divided into the Vehicle group (rats infused with the solvent used for dissolving A beta) and the A beta1-40-infused rat group (A beta group), whereas the 0.5% PE group was divided into the PE+Vehicle group (PE-preadministered vehicle-infused rats) and the PE+A beta group (PE-preadministered A beta-infused rats). A beta1-40 or vehicle was infused into the cerebral ventricle using a mini osmotic pump. Behavioral changes in the rats were assessed by an eight-arm radial maze. PE administration for 26 weeks significantly decreased the A beta-induced increase in the number of reference and working memory errors, with a concomitant reduction of hippocampal lipid peroxide (LPO; 40%) and cortico-hippocampal reactive oxygen species (ROS; 42% and 50%, respectively). Significantly reduced levels of LPO in the plasma (24%) and hippocampus (25%) as well as those of ROS in the hippocampus (23%) and cortex (41%) were found in the PE+Vehicle group as compared with the Vehicle group. Furthermore, rats with preadministered PE had higher ferric-reducing antioxidation power of plasma as compared with the Vehicle group. Our results suggest that long-term administration of green tea catechins provides effective prophylactic benefits against A beta-induced cognitive impairment by increasing antioxidative defenses.
机译：淀粉样蛋白β肽（A beta）诱导的氧化应激参与阿尔茨海默病（AD）的发病机理。相反，绿茶儿茶素赋予脑神经元有效的抗氧化防御作用。因此，我们研究了绿茶儿茶素[Polyphenon E（PE）：表没食子儿茶素3-没食子酸酯63％，表儿茶素的11％，（-）-表没食子儿茶素6％和（-）-6％的长期服用[epicatechin-gallate]可以预防AD动物模型的认知障碍，在大鼠脑室中注入A beta1-40。五周大的饲喂MF饮食的雄性Wistar大鼠随机分为两组：0.0％PE（仅用水大鼠）和0.5％PE（大鼠5 g / L PE）。给予PE后20周，将0.0％的PE组分为媒介物组（注入溶解Abeta的溶剂的大鼠）和注入Abeta1-40的大鼠组（A beta组），而将0.5％ PE组分为PE +车辆组（PE预先注入媒介物的大鼠）和PE + A beta组（PE预先注入Aβ的大鼠）。使用微型渗透泵将beta1-40或媒介物注入脑室。通过八臂径向迷宫评估大鼠的行为变化。 PE给药26周显着降低了Aβ引起的参考和工作记忆错误次数的增加，同时减少了海马脂质过氧化物（LPO; 40％）和皮质-海马活性氧（ROS; 42％和50％）。与车辆相比，PE +车辆组的血浆（24％）和海马（25％）的LPO水平显着降低，海马（23％）和皮质（41％）的ROS水平显着降低组。此外，与媒介物组相比，预先给予PE的大鼠血浆中的铁还原抗氧化能力更高。我们的研究结果表明，长期服用绿茶儿茶素可通过增加抗氧化防御作用来有效预防Aβ诱导的认知障碍。

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