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

Author:

Xie Chuan1,Yi Jian12,Lu Jing13,Nie Muwen4,Huang Meifang15,Rong Jianfang1,Zhu Zhenhua1,Chen Jiang1,Zhou Xiaoliang13,Li Bimin1,Chen Haiming1,Lu Nonghua1ORCID,Shu Xu1ORCID

Affiliation:

1. Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China

2. Department of Gastroenterology, Yichun People’s Hospital, Yichun, Jiangxi 336000, China

3. Department of Rheumatology, Ganzhou People’s Hospital, Ganzhou, Jiangxi 341000, China

4. Queen Mary Institute, Nanchang University, Nanchang, Jiangxi 330000, China

5. Department of Gastroenterology, Shangrao People’s Hospital, Ganzhou, Jiangxi 334000, China

Abstract

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.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

Cell Biology,Aging,General Medicine,Biochemistry

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