Taxifolin ameliorates IL-17A-enhanced hippocampal inflammation and oxidative stress in arsenic-exposed HT-22 cells

Abstract

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.