1 Department of Physiology, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, Turkey.
2 Department of Biophysics, Faculty of Medicine, Ataturk University, Erzurum, Turkey.
Research Article
World Journal of Advanced Research and Reviews, 2023, 19(02), 1318-1324
Received on 09 July 2023; revised on 25 August 2023; accepted on 28 August 2023
Arsenic (As) promotes neuronal damage in the hippocampus which is associated with cognitive function. Taxifolin, a flavonol with strong anti-oxidative and anti-inflammatory properties, is known to have beneficial properties in neurodegeneration, but its effect on As-induced hippocampal damage is unknown. Here, we explored whether taxifolin has therapeutic potential in ameliorating as causing toxicity in mouse hippocampal HT-22 cells, hypothesizing that inhibiting oxido-inflammation stress may reverse As-associated damage through several pathways. Findings indicate that pretreatment with taxifolin reversed the reduction of sodium arsenite (NaAsO2) induced cell death. In addition, taxifolin ameliorated NaAsO2-related oxidative stress as measured by the formation of ROS, MDA level and GSH content. Moreover, we revealed the taxifolin treatment resulted in a reduction of IL-17A level and subsequent diminished activation of TNF-α, IL-1β, and IL-6 concentrations in HT-22 cells treated with NaAsO2. These findings imply when considered collectively, HT-22 cells are shielded by taxifolin from NaAsO2-evoked oxidative cell death and neuroinflammation. Thus, our report indicates that has a protective role in hippocampal cell culture systems.
Arsenic; Hippocampus; Inflammation; Neurotoxicity; Oxidative damage
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Betul Cicek and Betul Danısman. Taxifolin ameliorates IL-17A-enhanced hippocampal inflammation and oxidative stress in arsenic-exposed HT-22 cells. World Journal of Advanced Research and Reviews, 2023, 19(2), 1318-1324. Article DOI: https://doi.org/10.30574/wjarr.2023.19.2.1661