National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun 130012, China.
Key Laboratory for Molecular Enzymology and Engineering, The Ministry of Education, School of Life Sciences, Jilin University, Changchun 130012, China.
Molecules. 2019 Feb 18;24(4):729. doi: 10.3390/molecules24040729.
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 () CL4176 expressing the human Aβ 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 (); 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 by reducing β-amyloid aggregation and inducing DAF-16 nuclear translocation that could activate the downstream signal pathway and enhance resistance to oxidative stress.
淀粉样蛋白-β(Amyloid-β)是阿尔茨海默病(AD)的标志之一,对神经元有毒性,并且还可能导致脑细胞死亡。氧化应激被认为在 AD 中起重要作用,并且有强有力的证据表明氧化应激与淀粉样蛋白-β有关。在本研究中,我们报告了紫竹普洱茶水提取物(ZTWE)和其主要成分(+)-儿茶素、咖啡因和原花青素混合物(MCCP)在 ZTWE 对表达人 Aβ基因的转基因()CL4176 诱导的β-淀粉样蛋白毒性的保护作用。ZTWE、(+)-儿茶素、咖啡因、原花青素和 MCCP 不同程度地延迟了β-淀粉样蛋白诱导的瘫痪。MCCP 处理不会影响淀粉样蛋白转基因()的转录丰度;然而,硫黄素 T 染色显示 Aβ 积累明显减少与未处理的蠕虫相比。使用转基因蠕虫进行的进一步研究发现,MCCP 促进了 DAF-16 从细胞质向细胞核的易位,并增加了超氧化物歧化酶 3(SOD-3)的表达。此外,MCCP 降低了 CL4176 蠕虫中的活性氧(ROS)含量并增加了 SOD 活性。总之,结果表明 MCCP 通过减少β-淀粉样蛋白聚集和诱导 DAF-16 核易位对β-淀粉样蛋白诱导的毒性具有显著的保护作用,这可能激活下游信号通路并增强对氧化应激的抵抗力。