期刊
TOXICOLOGY LETTERS
卷 282, 期 -, 页码 100-108出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.toxlet.2017.10.021
关键词
Autophagy; Oxidative stress; Apoptosis; 3-MA; A beta 1-42
类别
资金
- National Natural Science Foundation of China [31771148, 11232005]
- 111 Project [B08011]
- China Postdoctoral Science Foundation [BS000056]
Alzheimer's disease (AD) is a chronic neurodegenerative disease, which is characterized by the extracellular deposition of beta-amyloid (A beta). Previous studies reported that resveratrol, a natural herbal compound isolated from grapes, could alleviate the development and progression of AD. However, the underlying mechanism is still unclear. In the study, amyloid beta-peptide1-42 (A beta 1-42) -treated the differentiated rat pheochromocytoma cell line (PC12) was chosen as an AD cellular model. Our data showed that resveratrol attenuated A beta 1-42-induced cell death and significantly enhanced mitophagy including an increase in acidic vesicular organelle number, LC3-II/LC3-I ratio, Parkin and Beclin-1 expression, and LC3 and TOMM20 co-localization in A beta 1-42-treated PC12 cells. However, 3-MA remarkably inhibited resveratrol-induced mitophagy. Resveratrol reduced apoptosis, decreased oxidative status and alleviated mitochondrial damage in A beta 1-42-treated PC12 cells. However, all of the protective effects were significantly blocked by 3-MA, suggesting that mitophagy was considerably involved in the neuroprotective effects of resveratrol via decreasing oxidative status. Our study suggests that mitophagy pathway may become a new targeted therapy to attenuate neuronal damage induced by AD.
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