期刊
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
卷 2021, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2021/7158444
关键词
-
类别
资金
- National Natural Science Foundation of China [81903971]
- Natural Science Foundation of Guangdong Province [2021A1515011470]
- National Key R&D Program of China [2018YFC2002500]
- General Program of China Postdoctoral Science Foundation [2018M643377]
- Guangdong Provincial Key Laboratory of Traditional Chinese Medicine Informatization [2021B1212040007]
This study primarily explores the effects of the combination of beta-asarone and ICA on clearing noxious proteins and reversing cognitive deficits, as well as the role of mitophagy in the pathogenesis of AD. Combined treatment with mitophagy inducers may represent a potential strategy for therapeutic intervention in AD.
beta-Asarone is the main constituent of Acorus tatarinowii Schott and exhibits important effects in diseases such as neurodegenerative and neurovascular diseases. Icariin (ICA) is a major active ingredient of Epimedium that has attracted increasing attention because of its unique pharmacological effects in degenerative disease. In this paper, we primarily explored the effects of the combination of beta-asarone and ICA in clearing noxious proteins and reversing cognitive deficits. The accumulation of damaged mitochondria and mitophagy are hallmarks of aging and age-related neurodegeneration, including Alzheimer's disease (AD). Here, we provide evidence that autophagy/mitophagy is impaired in the hippocampus of APP/PS1 mice and in A beta 1-42-induced PC12 cell models. Enhanced mitophagic activity has been reported to promote A beta and tau clearance in in vitro and in vivo models. Meanwhile, there is growing evidence that treatment of AD should be preceded by intervention before the formation of pathological products. The efficacy of the combination therapy was better than that of the individual therapies applied separately. Then, we found that the combination therapy also inhibited cell and mitochondrial damage by inducing autophagy/mitophagy. These findings suggest that impaired removal of defective mitochondria is a pivotal event in AD pathogenesis, and that combination treatment with mitophagy inducers represents a potential strategy for therapeutic intervention.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据