Cyanidin-3-O-glucoside protects human gastric epithelial cells against Helicobacter pylori lipopolysaccharide-induced disorders by modulating TLR-mediated NF-κB pathway

Abstract

Helicobacter pylori (HP) contributes to the development of gastrointestinal disorders. Cyanidin-3-O-glucoside (C3G) is a major anthocyanin in human diets. In the current study, the effects and associated mechanism of C3G on HP lipopolysaccharide (LPS)-induced symptoms on human gastric epithelial cell (HGEC) cells were explored. The cells were exposed to LPS and C3G, and cellular viability, apoptotic rate, inflammation level, and toll-like receptor (TLR)-mediated nuclear factor-kappa B (NF-κB) pathway activity were measured. C3G suppressed the abnormal DNA synthesis and induced apoptosis in LPS-treated HGEC cells. C3G also reduced inflammation in LPS-treated HGEC cells. Although C3G exposure reduced the expressions of TLR2 and TLR4, it had no influence on TLR5. C3G deactivated TLR-mediated NF-κB signaling. The effects of C3G were stronger than anthocyanin extract but weaker than curcumin. The protective effects of C3G against HP LPS-induced injuries in gastric epithelial cells were associated with the deactivation of TLR2- and TLR4-mediated NF-κB signaling.

Keywords

• Cyanidin-3-O-glucoside
• Gastric epithelial cells
• Helicobacter pylori
• Lipopolysaccharide
• Toll-like receptor