Ingredients in Zijuan Pu'er Tea Extract Alleviate -Amyloid Peptide Toxicity in a Caenorhabditis elegans Model of Alzheimer's Disease Likely through DAF-16

被引:28
作者
Du, Fangzhou [1 ]
Zhou, Lin [1 ]
Jiao, Yan [1 ]
Bai, Shuju [1 ]
Wang, Lu [1 ]
Ma, Junfeng [1 ,2 ]
Fu, Xueqi [1 ,2 ]
机构
[1] Jilin Univ, Sch Life Sci, Natl Engn Lab AIDS Vaccine, Changchun 130012, Jilin, Peoples R China
[2] Jilin Univ, Sch Life Sci, Key Lab Mol Enzymol & Engn, Minist Educ, Changchun 130012, Jilin, Peoples R China
来源
MOLECULES | 2019年 / 24卷 / 04期
基金
中国国家自然科学基金;
关键词
Alzheimer's disease; oxidative stress; C; elegans; amyloid-; STRESS RESISTANCE; OXIDATIVE STRESS; C-ELEGANS; A-BETA; PARALYSIS;
D O I
10.3390/molecules24040729
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Amyloid-, 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-. 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 -amyloid-induced toxicity in transgenic Caenorhabditis elegans (C. elegans) CL4176 expressing the human A(1-42) gene. ZTWE, (+)-catechins, caffeine, procyanidin and MCCP delayed the -amyloid-induced paralysis to different degrees. The MCCP treatment did not affect the transcript abundance of amyloid- transgene (amy-1); however, Thioflavin T staining showed a significant decrease in A 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 -amyloid-induced toxicity in C. elegans by reducing -amyloid aggregation and inducing DAF-16 nuclear translocation that could activate the downstream signal pathway and enhance resistance to oxidative stress.
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页数:14
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