ISSN: 1449-1907International Journal of Medical Sciences
Global reach, higher impact
Int J Med Sci 2014; 11(7):742-747. doi:10.7150/ijms.7167 This issue Cite
Short Research Communication
Cyanidin 3-O-Glucoside Reduces Helicobacter pylori VacA-Induced Cell Death of Gastric KATO III Cells through Inhibition of the SecA Pathway
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;
3. Department of Clinical Laboratory Science, Hyegeon College, Hongseong 350-702, Republic of Korea;
4. Department of Functional Crops, National Institute of Crop Science, Rural Development Administration, Miryang 627-803, Republic of Korea.
* These investigators contributed equally to this study.
Abstract
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.
Keywords: H. pylori, cyanidin 3-O-glucoside, VacA secretion