Abstract
Accumulation of β-amyloid (Aβ) causes oxidative stress, which is the major pathological mechanism in Alzheimer’s disease (AD). β-asarone could reduce Aβ-induced oxidative stress and neuronal damage, but the molecular mechanism remains elusive. In this study, we used an Aβ-stimulated PC12 cell model to explore the neuroprotective effects and potential mechanisms of β-asarone. The results showed that β-asarone could improve cell viability and weaken cell damage and apoptosis. β-asarone could also decrease the level of ROS and MDA; increase the level of SOD, CAT, and GSH-PX; and ameliorate the mitochondrial membrane potential. Furthermore, β-asarone could promote the expression of Nrf2 and HO-1 by upregulating the level of PI3K/Akt phosphorylation. In conclusion, β-asarone could exert neuroprotective effects by modulating the P13K/Akt/Nrf2 signaling pathway. β-asarone might be a promising therapy for AD.
Highlights
Alzheimer’s disease (AD) is the most common neurodegenerative disease and the primary cause of dementia in elderly people
Numerous pieces of evidence suggested that mitochondria dysfunction and oxidative stress were involved in AD pathogenesis and progression (Wang et al, 2014; Tobore, 2019)
We focused on the effect of β-asarone on the cell apoptosis, reactive oxygen species (ROS), and mitochondria dysfunction in PC12 cells
Summary
Alzheimer’s disease (AD) is the most common neurodegenerative disease and the primary cause of dementia in elderly people. The neuropathology of AD includes accumulation of β-amyloid (Aβ), neurofibrillary tangles, and loss of neurons (Scarpini et al, 2003). Numerous pieces of evidence suggested that mitochondria dysfunction and oxidative stress were involved in AD pathogenesis and progression (Wang et al, 2014; Tobore, 2019). Previous studies showed that the deposition of Aβ caused the production of reactive oxygen species (ROS) and mitochondria dysfunction, which can induce oxidative stress and neuronal apoptosis (Habib et al, 2010; Huang et al, 2012; Butterfield et al, 2013; Bhat et al, 2015). It might be helpful to inhibit Aβ-mediated oxidative stress for the prevention and treatment of AD
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