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Eur J Pharmacol. 2014 Oct 15;741:195-204. doi: 10.1016/j.ejphar.2014.08.006. Epub 2014 Aug 23.

Beta-asarone attenuates amyloid beta-induced autophagy via Akt/mTOR pathway in PC12 cells.

Author information

1
The First Affiliated Hospital of Guangzhou University of Chinese Medicine, 16, Jichang Road, 510405 Guangzhou, China; Sanya Traditional Chinese Medicine Hospital, 106, Fenghuang Road, 572000 Sanya, China. Electronic address: xuezhongfeng@foxmail.com.
2
The First Affiliated Hospital of Guangzhou University of Chinese Medicine, 16, Jichang Road, 510405 Guangzhou, China; Sanya Traditional Chinese Medicine Hospital, 106, Fenghuang Road, 572000 Sanya, China. Electronic address: 770217837@qq.com.
3
The First Affiliated Hospital of Guangzhou University of Chinese Medicine, 16, Jichang Road, 510405 Guangzhou, China. Electronic address: Loveguangzhou2009@163.com.
4
The First Affiliated Hospital of Guangzhou University of Chinese Medicine, 16, Jichang Road, 510405 Guangzhou, China. Electronic address: xiaoyinlan@126.com.
5
The First Affiliated Hospital of Guangzhou University of Chinese Medicine, 16, Jichang Road, 510405 Guangzhou, China. Electronic address: heyuping@163.com.
6
The First Affiliated Hospital of Guangzhou University of Chinese Medicine, 16, Jichang Road, 510405 Guangzhou, China. Electronic address: zgmfx24a@163.com.
7
The First Affiliated Hospital of Guangzhou University of Chinese Medicine, 16, Jichang Road, 510405 Guangzhou, China. Electronic address: fangyq2@163.com.

Abstract

Alzheimer's disease (AD) is an age related and progressive neurodegenerative disease. Autophagy is a self-degradative process and plays a critical role in removing long-lived proteins and damaged organelles. Recent evidence suggests that autophagy might be involved in the pathogenesis of AD. β-asarone have various neuroprotective effects. However, the effect of β-asarone on autophagy in amyloid β-peptide (Aβ) induced cell injury is unclear, and little is known about the signaling pathway of β-asarone in autophagy regulation. The aim of the present study was to determine whether β-asarone protects cells from Aβ1-42 induced cytotoxicity via regulation of Beclin-1 dependent autophagy and its regulating signaling pathway. We examined effects of β-asarone on cell morphology, cell viability, neuron specific enolase (NSE) levels, autophagosomes and regulating Beclin-1, p-Akt and p-mTOR expressions in Aβ1-42 treated PC12 cells. We found that β-asarone could maintain the original morphology of cells and increase cell viability and decrease NSE levels significantly. Meanwhile, β-asarone decreased Beclin-1 expression significantly. In addition, β-asarone can increase levels of p-Akt and p-mTOR. These results showed that β-asarone protected cells from Aβ1-42 induced cytotoxicity and attenuated autophagy via activation of Akt-mTOR signaling pathway, which could be involved in neuroprotection of β-asarone against Aβ toxicity. Our findings suggest that β-asarone might be a potential preventive drug for AD.

KEYWORDS:

3-methyladenine (PubChem CID: 1673); Akt; Alzheimer′s disease; Autophagy; Beclin-1; Beta-asarone; Beta-asarone (PubChem CID: 5281758); Mammalian target of rapamycin; NVP-BEZ235 (PubChem CID: 11977753); Rapamycin (PubChem CID: 5284616)

PMID:
25160744
DOI:
10.1016/j.ejphar.2014.08.006
[Indexed for MEDLINE]

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