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Int J Med Sci. 2014 May 14;11(7):742-7. doi: 10.7150/ijms.7167. eCollection 2014.

Cyanidin 3-O-glucoside reduces Helicobacter pylori VacA-induced cell death of gastric KATO III cells through inhibition of the SecA pathway.

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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.


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.


H. pylori; VacA secretion; cyanidin 3-O-glucoside

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