L-ascorbic Acid-2-Glucoside inhibits Helicobacter pylori-induced apoptosis through mitochondrial pathway in Gastric Epithelial cells

Abstract

Helicobacter pylori (H. pylori) infection is the major cause for gastritis, peptic ulcer, and gastric cancer. Elevated oxidative stress, mitochondrial dysfunction and apoptotic death of gastric epithelial cells are typical hallmarks of H. pylori infection. Ascorbic Acid 2-Glucoside (AA2G) is a stable version of Vitamin C, that binds glucose to conventional vitamin C. AA2G has free radical scavenging activities and anti-apoptotic abilities. However, the protective effect of AA2G against H. pylori-infection in gastric epithelial cells is yet unknown. In this study, we investigated the effects of AA2G in human H. pylori-infected gastric epithelial cells. AA2G could remarkably ameliorate H. pylori-induced oxidative stress, including the levels of intracellular reactive oxygen species (ROS) and 4-hydroxynonenal (4-HNE). Importantly, AA2G treatment also improved mitochondrial function by restoring the level of ATP and mitochondrial membrane potential (MMP). Furthermore, AA2G reduced apoptosis induced by H. pylori through modulation of mitochondria-dependent apoptotic pathways. Our findings suggest that AA2G has a protective effect against H. pylori infection in gastric epithelial cells.

Keywords: Apoptosis; Ascorbic acid 2-Glucoside (AA2G); Gastric epithelial cells; Helicobacter pylori; Oxidative stress.