Thermal cycling protects SH-SY5Y cells against hydrogen peroxide and β-amyloid-induced cell injury through stress response mechanisms involving Akt pathway
Journal
PLoS ONE
Journal Volume
15
Journal Issue
10-Oct
Pages
-
Date Issued
2020
Author(s)
Abstract
Neurodegenerative diseases (NDDs) are becoming a major threat to public health, according to the World Health Organization (WHO). The most common form of NDDs is Alzheimer’s disease (AD), boasting 60–70% share. Although some debates still exist, excessive aggregation of β-amyloid protein (Aβ) and neurofibrillary tangles has been deemed one of the major causes for the pathogenesis of AD. A growing number of evidences from studies, however, have suggested that reactive oxygen species (ROS) also play a key role in the onset and progression of AD. Although scientists have had some understanding of the pathogenesis of AD, the disease still cannot be cured, with existing treatment only capable of providing a temporary relief at best, partly due to the obstacle of blood-brain barrier (BBB). The study was aimed to ascertain the neuroprotective effect of thermal cycle hyperthermia (TC-HT) against hydrogen peroxide (H2O2) and Aβ-induced cytotoxicity in SH-SY5Y cells. Treating cells with this physical stimulation beforehand significantly improved the cell viability and decreased the ROS content. The underlying mechanisms may be due to the activation of Akt pathway and the downstream antioxidant and prosurvival proteins. The findings manifest significant potential of TC-HT in neuroprotection, via inhibition of oxidative stress and cell apoptosis. It is believed that coupled with the use of drugs or natural compounds, this methodology can be even more effective in treating NDDs. ? 2020 Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
SDGs
Other Subjects
amyloid beta protein; hydrogen peroxide; protein kinase B; reactive oxygen metabolite; amyloid beta protein; cyclic AMP responsive element binding protein; heat shock protein; hydrogen peroxide; insulinase; matrix metalloproteinase; NFE2L2 protein, human; proteasome; protein kinase B; transcription factor Nrf2; apoptosis; Article; cell damage; cell protection; cell survival; cell viability; cellular stress response; controlled study; cytotoxicity; human; human cell; hyperthermia; in vitro study; mitochondrial membrane potential; nerve degeneration; neuroprotection; oxidative stress; SH-SY5Y cell line; signal transduction; drug effect; gene expression regulation; metabolism; signal transduction; thermotherapy; tumor cell line; Amyloid beta-Peptides; Cell Line, Tumor; Cyclic AMP Response Element-Binding Protein; Gene Expression Regulation; Heat-Shock Proteins; Humans; Hydrogen Peroxide; Hyperthermia, Induced; Insulysin; Matrix Metalloproteinases; NF-E2-Related Factor 2; Oxidative Stress; Proteasome Endopeptidase Complex; Proto-Oncogene Proteins c-akt; Signal Transduction
Type
journal article