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Background    H. pylori  infection induces reactive oxygen species- (ROS-) related DNA damage and activates the PI3K/Akt pathway in gastric epithelial cells.  N -Acetylcysteine (NAC) is known as an inhibitor of ROS; the role of NAC in  H. pylori -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  H. pylori -related diseases.Method   An  in vitro  coculture system and an  in vivo  Balb/c mouse model of  H. pylori -infected gastric epithelial cells were established. The effects of  H. pylori  infection 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  N -acetylcysteine (NAC) was also evaluated with  in vitro  and  in vivo H. pylori  infection models.Results   The results revealed that,  in vitro  and  in vivo ,  H. pylori  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.  H. pylori  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, chronic  H. pylori  infection decreased APE-1 expression in the gastric mucosa of Balb/c mice.Conclusions   An increased ROS level is a critical mechanism in  H. pylori  pathogenesis, and NAC may be beneficial for the treatment of  H. pylori -related gastric diseases linked to oxidative DNA damage.

N-Acetylcysteine Reduces ROS-Mediated Oxidative DNA Damage and PI3K/Akt Pathway Activation Induced by Helicobacter pylori Infection