Accumulation of Deleterious Effects in Gastric Epithelial Cells and Vascular Endothelial Cells In Vitro in the Milieu of Helicobacter pylori Components, 7-Ketocholesterol and Acetylsalicylic Acid

The Gastric pathogen Helicobacter pylori (HP) may influence the development of coronary heart disease (CHD). H. pylori induce reactive oxygen species (ROS), which transform cholesterol to 7-ketocholesterol (7-kCh), a CHD risk factor. Acetylsalicylic acid (ASA)-an Anti-aggregation drug used in CHD patients-may increase gastric bleeding and inflammation. We examined whether H. pylori driven ROS effects in the cell cultures of gastric epithelial cells (AGS) and vascular endothelial cells (HUVEC) progress in the milieu of 7-kCh and ASA. Cell cultures, exposed to 7-kCh or ASA alone or pulsed with the H. pylori antigenic complex-Glycine acid extract (GE), urease (UreA), cytotoxin associated gene A (CagA) protein or lipopolysaccharide (LPS), alone or with 7-kCh and ASA-were examined for ROS, apoptosis, cell integrity, interleukin (IL)-8, the activation of signal transducer, the activator of transcription 3 (STAT3), and wound healing. ASA and 7-kCh alone, and particularly in conjunction with H. pylori components, increased the ROS level and the rate of apoptosis, which was followed by cell disintegration, the activation of STAT3, and IL-8 elevation. AGS cells were unable to undergo wound healing. The cell ROS response to H. pylori components may be elevated by 7-kCh and ASA.

Automated summary

The gastric pathogen Helicobacter pylori has been found to influence the development of coronary heart disease (CHD) by inducing reactive oxygen species (ROS) and transforming cholesterol into 7-ketocholesterol (7-kCh). This study examined the effects of H. pylori components, in the presence of 7-kCh and acetylsalicylic acid (ASA), on gastric epithelial cells and vascular endothelial cells. The results showed that ASA and 7-kCh, especially in conjunction with H. pylori components, increased ROS levels, apoptosis, cell disintegration, activation of STAT3, and elevation of IL-8. AGS cells were unable to undergo wound healing. The findings suggest that the ROS response to H. pylori components may be enhanced by 7-kCh and ASA.