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Title: Neuroprotective Effects of Phenolic and Carboxylic Acids on Oxidative Stress-Induced Toxicity in Human Neuroblastoma SH-SY5Y Cells
Authors: Naw Hser Gay
Kamonrat Phopin
Wilasinee Suwanjang
Napat Songtawee
Waralee Ruankham
Prapimpun Wongchitrat
Supaluk Prachayasittikul
Virapong Prachayasittikul
Mahidol University
University of Medical Technology
Keywords: Biochemistry, Genetics and Molecular Biology;Neuroscience
Issue Date: 1-Mar-2018
Citation: Neurochemical Research. Vol.43, No.3 (2018), 619-636
Abstract: © 2018, Springer Science+Business Media, LLC, part of Springer Nature. An increase in oxidative stress is a key factor responsible for neurotoxicity induction and cell death leading to neurodegenerative diseases including Parkinson’s and Alzheimer’s diseases. Plant phenolics exert diverse bioactivities i.e., antioxidant, anti-inflammatory, and neuroprotective effects. Herein, phenolic compounds, namely protocatechuic aldehyde (PCA) constituents of Hydnophytum formicarum Jack. including vanillic acid (VA) and trans-ferulic acid (FA) found in Spilanthes acmella Murr., were explored for anti-neurodegenerative properties using an in vitro model of oxidative stress-induced neuroblastoma SH-SY5Y cells. Exposure of the neuronal cells with H 2 O 2 resulted in the decrease of cell viability, but increasing in the level of reactive oxygen species (ROS) together with morphological changes and inducing cellular apoptosis. SH-SY5Y cells pretreated with 5 µM of PCA, VA, and FA were able to attenuate cell death caused by H 2 O 2 -induced toxicity, as well as decreased ROS level and apoptotic cells after 24 h of treatment. Pretreated SH-SY5Y cells with phenolic compounds also helped to upregulate H 2 O 2 -induced depletion of the expressions of sirtuin-1 (SIRT1) and forkhead box O (FoxO) 3a as well as induce the levels of antioxidant (superoxide dismutase (SOD) 2 and catalase) and antiapoptotic B-cell lymphoma 2 (Bcl-2) proteins. The findings suggest that these phenolics might be promising compounds against neurodegeneration.
ISSN: 15736903
Appears in Collections:Scopus 2018

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