Evidence map›Paper›PMID 24904230›Full record

ArticleInternational journal of medical sciences2014

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

Open access · goldAbstract read
In one paragraph

Article in International journal of medical sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 28 citations in OpenAlex.

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  7. Fighting the Antibiotic Crisis: Flavonoids as Promising Antibacterial Drugs AgainstFrontiers in cellular and infection microbiology · 2021
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  8. Inhibitory Effects of β-Caryophyllene onInternational journal of molecular sciences · 2020
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  10. Inhibitory Effects of Menadione onInternational journal of molecular sciences · 2019
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  11. ProbioticJournal of clinical medicine · 2019
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  12. Review
  13. Review
  14. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Sa-Hyun Kim1. Department of Clinical Laboratory Science, Semyung University, Jaecheon 390-711, Republic of Korea;
Hyunjun Woo2. Department of Biomedical Laboratory Science, College of Health Science, Yonsei University, Wonju 220-710, Republic of Korea;
Min Park2. Department of Biomedical Laboratory Science, College of Health Science, Yonsei University, Wonju 220-710, Republic of Korea;
Ki-Jong Rhee2. Department of Biomedical Laboratory Science, College of Health Science, Yonsei University, Wonju 220-710, Republic of Korea;
Cheol Moon1. Department of Clinical Laboratory Science, Semyung University, Jaecheon 390-711, Republic of Korea;
Dongsup Lee3. Department of Clinical Laboratory Science, Hyegeon College, Hongseong 350-702, Republic of Korea;
Woo Duck Seo4. Department of Functional Crops, National Institute of Crop Science, Rural Development Administration, Miryang 627-803, Republic of Korea.
Jong Bae Kim2. Department of Biomedical Laboratory Science, College of Health Science, Yonsei University, Wonju 220-710, Republic of Korea;
Yonsei University · KRSemyung University · KRHyejeon College · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Adenosine TriphosphatasesAnthocyaninsBacterial ProteinsCell DeathCell LineEpithelial CellsGastric MucosaGlucosidesHelicobacter pyloriHumansMembrane Transport ProteinsSecA ProteinsSEC Translocation ChannelsSignal TransductionAdenosine TriphosphatasesAnthocyaninsBacterial Proteinscyanidin-3-O-beta-glucopyranosideGlucosidesMembrane Transport ProteinsSecA ProteinsSEC Translocation ChannelsVacA protein, Helicobacter pyloricyanidin 3-O-glucosideH. pyloriVacA secretion

Identifiers

PMID24904230
PMCPMC4045794
OpenAlexW2039975792

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.