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.

幽门螺杆菌（HP）有助于胃肠道疾病的发展。氰基-3-O-葡萄糖苷（C3G）是人类饮食中的主要花色苷。在当前的研究中，探讨了C3G对HP脂多糖（LPS）诱导的人胃上皮细胞（HGEC）细胞症状的影响及其相关机制。将细胞暴露于LPS和C3G，并测量细胞活力，凋亡率，炎症水平和toll样受体（TLR）介导的核因子-κB（NF-κB）通路活性。C3G抑制LPS处理的HGEC细胞中异常的DNA合成并诱导凋亡。C3G还可以减轻LPS处理的HGEC细胞的炎症。尽管C3G暴露降低了TLR2和TLR4的表达，但对TLR5没有影响。C3G使TLR介导的NF-κB信号失活。C3G的作用强于花青素提取物，但弱于姜黄素。C3G对HP LPS诱导的胃上皮细胞损伤的保护作用与TLR2和TLR4介导的NF-κB信号的失活有关。