脂质运载蛋白
福克斯O1
生物
基因敲除
超氧化物歧化酶
丙二醛
小RNA
癌症研究
氧化应激
药理学
细胞生物学
内分泌学
生物化学
信号转导
基因
蛋白激酶B
作者
Bowen Wu,Jin‐Dong Guo,Mi-Shan Wu,Yu Liu,Meng Lü,Yuhui Zhou,Hongwei Han
出处
期刊:Epigenomics
[Future Medicine]
日期:2020-09-01
卷期号:12 (17): 1501-1513
被引量:16
标识
DOI:10.2217/epi-2019-0215
摘要
Aim: Alzheimer's disease (AD) is the most frequent cause of dementia and characterized by the accumulation of β-amyloid peptides in plaques and vessel walls. This study proposed a hypothesis of an inhibitory role of miR-96-5p in AD via regulating Foxo1. Methods & methods: AD mouse models were established by injecting with 1% pentobarbital. Results: Knockdown of miR-96-5p in the presence of naringin was shown to reduce the expression of Foxo1 and contents of superoxide dismutase, catalase and glutathione peroxidase, yet increase lipocalin-2 expression as well as hydroxyproline and malondialdehyde contents. Also, Foxo1-mediated lipocalin-2 inhibition attenuated AD. Conclusion: Our study shows downregulating miR-96-5p limited AD progression, highlighting miR-96-5p a potential therapeutic target in treating AD.
科研通智能强力驱动
Strongly Powered by AbleSci AI