首页> 美国卫生研究院文献>Molecules >Ingredients in Zijuan Pu’er Tea Extract Alleviate β-Amyloid Peptide Toxicity in a Caenorhabditis elegans Model of Alzheimer’s Disease Likely through DAF-16
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Ingredients in Zijuan Pu’er Tea Extract Alleviate β-Amyloid Peptide Toxicity in a Caenorhabditis elegans Model of Alzheimer’s Disease Likely through DAF-16

机译:紫娟普’茶提取物中的成分可能通过DAF-16减轻了阿尔茨海默氏病秀丽隐杆线虫模型中的β-淀粉样肽毒性

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摘要

Amyloid-β, one of the hallmarks of Alzheimer’s disease (AD), is toxic to neurons and can also cause brain cell death. Oxidative stress is known to play an important role in AD, and there is strong evidence that oxidative stress is associated with amyloid-β. In the present study we report the protective effect of Zijuan Pu’er tea water extract (ZTWE) and the mixture of main ingredients (+)-catechins, caffeine and procyanidin (MCCP) in ZTWE on β-amyloid-induced toxicity in transgenic Caenorhabditis elegans (C. elegans) CL4176 expressing the human Aβ1–42 gene. ZTWE, (+)-catechins, caffeine, procyanidin and MCCP delayed the β-amyloid-induced paralysis to different degrees. The MCCP treatment did not affect the transcript abundance of amyloid-β transgene (amy-1); however, Thioflavin T staining showed a significant decrease in Aβ accumulation compared to untreated worms. Further research using transgenic worms found that MCCP promoted the translocation of DAF-16 from cytoplasm to nucleus and increased the expression of superoxide dismutase 3 (SOD-3). In addition, MCCP decreased the reactive oxygen species (ROS) content and increased the SOD activity in CL4176 worms. In conclusion, the results suggested that MCCP had a significant protective effect on β-amyloid-induced toxicity in C. elegans by reducing β-amyloid aggregation and inducing DAF-16 nuclear translocation that could activate the downstream signal pathway and enhance resistance to oxidative stress.
机译:淀粉样蛋白-β是阿尔茨海默氏病(AD)的标志之一,对神经元有毒,还可能导致脑细胞死亡。已知氧化应激在AD中起重要作用,并且有充分的证据表明氧化应激与淀粉样β相关。在本研究中,我们报告了紫娟普'茶水提取物(ZTWE)和主要成分(+)-儿茶素,咖啡因和原花青素(MCCP)的混合物对β-淀粉样蛋白引起的转基因Caenorhabditis毒性的保护作用秀丽隐杆线虫(CL。elegans)表达人类Aβ1-42基因。 ZTWE,(+)-儿茶素,咖啡因,原花青素和MCCP在不同程度上延迟了β-淀粉样蛋白引起的麻痹。 MCCP处理不影响淀粉样β转基因(amy-1)的转录本丰度。然而,硫黄素T染色显示与未经处理的蠕虫相比,Aβ积累显着降低。使用转基因蠕虫的进一步研究发现,MCCP促进了DAF-16从细胞质到细胞核的转运,并增加了超氧化物歧化酶3(SOD-3)的表达。此外,MCCP降低了CL4176蠕虫的活性氧(ROS)含量并增加了SOD活性。总之,结果表明MCCP通过减少β淀粉样蛋白聚集并诱导DAF-16核易位,从而激活下游信号通路并增强对氧化应激的抵抗力,从而对秀丽隐杆线虫的β-淀粉样蛋白毒性具有显着的保护作用。 。

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