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

Sa Hyun Kim, Hyunjun Woo, Min Park, Ki Jong Rhee, Cheol Moon, Dongsup Lee, Woo Duck Seo, Jong Bae Kim

Research output: Contribution to journalArticle

11 Citations (Scopus)

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 caspa-se-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.

Original languageEnglish
Pages (from-to)742-747
Number of pages6
JournalInternational Journal of Medical Sciences
Volume11
Issue number7
DOIs
Publication statusPublished - 2014 May 14

All Science Journal Classification (ASJC) codes

  • Medicine(all)

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