1. Department of Clinical Laboratory Science, Semyung University, Jaecheon 390-711, Republic of Korea;
2. Department of Biomedical Laboratory Science, College of Health Science, Yonsei University, Wonju 220-710, Republic of Korea;
Int J Med Sci. 2014 May 14;11(7):742-7. doi: 10.7150/ijms.7167. eCollection 2014.
Two key virulence factors of Helicobacter pylori are the secreted virulent proteins of vacuolating toxin A (VacA) and cytotoxin associated protein A (CagA) which lead to damages of gastric epithelial cells. We previously identified that the cyanidin 3-O-glucoside (C3G) inhibits the secretion of both VacA and CagA. In the current report, we show that C3G inhibits VacA secretion in a dose-dependent manner by inhibiting secretion system subunit protein A (SecA) synthesis. As SecA is involved in translocation of bacterial proteins, we predicted that inhibition of the SecA pathway by C3G should decrease H. pylori-induced cell death. To test this hypothesis, the human gastric cell line KATO III cells were co-cultured with H. pylori 60190 (VacA(+)/CagA(+)) and C3G. We found that C3G treatment caused a decrease in activation of the pro-apoptotic proteins caspase-3/-8 in H. pylori-infected cells leading to a decrease in cell death. Our data suggest that consumption of foods containing anthocyanin may be beneficial in reducing cell damage due to H. pylori infection.
幽门螺杆菌的两个主要毒力因子是VacA（空泡毒素 A）和CagA（细胞毒素相关蛋白 A）这两种分泌的毒性蛋白，它们会导致胃上皮细胞损伤。我们之前已经确定矢车菊素 3-O-葡萄糖苷（C3G）可以抑制 VacA 和 CagA 的分泌。在本报告中，我们发现 C3G 通过抑制分泌系统亚基蛋白 A（SecA）的合成，以剂量依赖的方式抑制 VacA 的分泌。由于 SecA 参与细菌蛋白的易位，我们预测 C3G 对 SecA 途径的抑制应该会减少 H. pylori 诱导的细胞死亡。为了验证这一假设，我们将人胃细胞系 KATO III 细胞与 H. pylori 60190（VacA(+)/CagA(+))共培养，并加入 C3G。我们发现 C3G 处理会导致 H. pylori 感染细胞中促凋亡蛋白 caspase-3/-8 的激活减少，从而导致细胞死亡减少。我们的数据表明，食用含有花青素的食物可能有助于减少 H. pylori 感染引起的细胞损伤。
