Abstract
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by progressive memory damage and cognitive dysfunction. Studies have shown that defective autophagic flux is associated with neuronal dysfunction. Modulating autophagic activity represents a potential method of combating AD. In Chinese medicine, Acori Tatarinowii Rhizoma is used to treat dementia and amnesia. β-Asarone, an active component of this rhizome can protect PC12 cells from Aβ-induced injury and modulate expression of autophagy factors. However, its cytoprotective mechanisms have yet to be discerned. It is unclear whether β-asarone affects autophagic flux and, if it does, whether this effect can alleviate Aβ cell damage. In the present study, we constructed APPswe-overexpressing PC12 cell line as a cell model of Aβ-induced damage and assessed expression of autophagic flux-related proteins as well as the number and morphology of autophagosomes and autolysosomes. Our results show that β-asarone decreases the expression levels of Beclin-1, p62, LC3-Ⅱ, and Aβ1-42. β-Asarone reduced the number of autophagosomes and increased the number of autolysosomes, as determined by confocal laser scanning microscopy and transmission electron microscopy. Our results suggest that β-asarone can protect PC12 cells from Aβ-induced damage by promoting autophagic flux, which may be achieved by enhancing autophagosome-lysosome fusion and/or lysosome function.
Highlights
Alzheimer’s disease (AD) is a chronic neurodegenerative disease with an insidious onset, and is clinically characterized by generalized dementia, such as memory loss, cognitive dysfunction, and a decline in self-care that leads to death (Cai et al, 2019)
To establish a cell injury model that is induced by Aβ, PC12 cells were infected with lentiviral particles containing APPswe, with an empty vector used to generate a control line
Gene and protein expression levels of amyloid precursor protein (APP) were detected by real-time PCR and western blot to confirm that these cell lines stably overexpressed APPswe
Summary
Alzheimer’s disease (AD) is a chronic neurodegenerative disease with an insidious onset, and is clinically characterized by generalized dementia, such as memory loss, cognitive dysfunction, and a decline in self-care that leads to death (Cai et al, 2019). Onset of AD is highly correlated with increasing age. With an aging population and a perpetually increasing life expectancy, the number of patients with AD worldwide has increased each year. In 2018, it was estimated that 50 million people worldwide were living with dementia, with AD accounting for 50–60% of these cases (Potashkin et al, 2019). Only five anti-AD drugs have been approved for clinical use by the United States Food and Drug Administration (FDA). These drugs only relieve symptoms but cannot reverse neuronal damage caused by AD (Isla et al, 2021). It is critical to understand the pathological mechanisms of AD and to find effective methods of prevention and treatment
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