-Acetylcysteine Reduces ROS-Mediated Oxidative DNA Damage and PI3K/Akt Pathway Activation Induced byInfection.
Oxid Med Cell Longev. 2018 ;2018:1874985. Epub 2018 Apr 26. PMID: 29854076
Background: infection induces reactive oxygen species- (ROS-) related DNA damage and activates the PI3K/Akt pathway in gastric epithelial cells.-Acetylcysteine (NAC) is known as an inhibitor of ROS; the role of NAC in-related diseases is unclear.
Aim: The aim of this study was to evaluate the role of ROS and the protective role of NAC in the pathogenesis of-related diseases.
Method: Ancoculture system and anBalb/c mouse model of-infected gastric epithelial cells were established. The effects ofinfection on DNA damage and ROS were assessed by the comet assay and fluorescent dichlorofluorescein assay. The level of PI3K/Akt pathway-related proteins was evaluated by Western blotting. The protective role of-acetylcysteine (NAC) was also evaluated withandinfection models.
Results: The results revealed that,and,infection increased the ROS level and induced DNA damage in gastric epithelial cells. NAC treatment effectively reduced the ROS level and inhibited DNA damage in GES-1 cells and the gastric mucosa of Balb/c mice.infection induced ROS-mediated PI3K/Akt pathway activation, and NAC treatment inhibited this effect. However, the gastric mucosa pathological score of the NAC-treated group was not significantly different from that of the untreated group. Furthermore, chronicinfection decreased APE-1 expression in the gastric mucosa of Balb/c mice.
Conclusions: An increased ROS level is a critical mechanism inpathogenesis, and NAC may be beneficial for the treatment of-related gastric diseases linked to oxidative DNA damage.