Evidence map›Paper›PMID 20179294›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2010

American ginseng suppresses colitis through p53-mediated apoptosis of inflammatory cells.

Yu Jin, Anne B Hofseth, Xiangli Cui, Anthony J Windust, Deepak Poudyal, Alex A Chumanevich, Lydia E Matesic, Narendra P Singh, Mitzi Nagarkatti, Prakash S Nagarkatti and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Article
  7. Panaxynol alleviates colorectal cancer in a murine model via suppressing macrophages and inflammation.American journal of physiology. Gastrointestinal and liver physiology · 2023
    Article
  8. Review
  9. Terahertz Spectroscopy for Accurate Identification ofPlant phenomics (Washington, D.C.) · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. American Ginseng (Nutrients · 2019
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

11 authors at 2 institutions in 1 country.

Yu JinDepartment of Biomedical and Pharmaceutical Sciences, South Carolina College of Pharmacy, 770 Sumter Street, Coker Life Sciences, University of South Carolina, Columbia, SC 29208, USA.
Anne B Hofseth
Xiangli Cui
Anthony J Windust
Deepak Poudyal
Alex A Chumanevich
Lydia E Matesic
Narendra P Singh
Mitzi Nagarkatti
Prakash S Nagarkatti
Lorne J Hofseth
University of South Carolina · USNational Academies of Sciences, Engineering, and Medicine · US

Funding

TISSUE BIOREPOSITORYP20RR017698 · NCRR · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI FAYAD, RAJA · 2002 to 2011
$22.5M
Use of Resveratrol to treat experimental multiple sclerosisP01AT003961 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI NAGARKATTI, PRAKASH S · 2007 to 2018
$14.2M
NCCIH NIH HHS 1P01AT003961-01A1NCCIH NIH HHS P01 AT003961NCRR NIH HHS P20 RR017698NCRR NIH HHS P20RR17698-01
6 · The paper itself

Abstract

Ulcerative colitis is a dynamic, chronic inflammatory condition associated with an increased colon cancer risk. Inflammatory cell apoptosis is a key mechanism regulating ulcerative colitis. American ginseng (AG) is a putative antioxidant that can suppress hyperactive immune cells. We have recently shown that AG can prevent and treat mouse colitis. Because p53 levels are elevated in inflammatory cells in both mouse and human colitis, we tested the hypothesis that AG protects from colitis by driving inflammatory cell apoptosis through a p53 mechanism. We used isogenic p53(+/+) and p53(-/-) inflammatory cell lines as well as primary CD4(+)/CD25(-) effector T cells from p53(+/+) and p53(-/-) mice to show that AG drives apoptosis in a p53-dependent manner. Moreover, we used a dextran sulfate sodium (DSS) model of colitis in C57BL/6 p53(+/+) and p53(-/-) mice to test whether the protective effect of AG against colitis is p53 dependent. Data indicate that AG induces apoptosis in p53(+/+) but not in isogenic p53(-/-) cells in vitro. In vivo, C57BL/6 p53(+/+) mice are responsive to the protective effects of AG against DSS-induced colitis, whereas AG fails to protect from colitis in p53(-/-) mice. Furthermore, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling of inflammatory cells within the colonic mesenteric lymph nodes is elevated in p53(+/+) mice consuming DSS + AG but not in p53(-/-) mice consuming DSS + AG. Results are consistent with our in vitro data and with the hypothesis that AG drives inflammatory cell apoptosis in vivo, providing a mechanism by which AG protects from colitis in this DSS mouse model.

Indexed as

PanaxPhytotherapyAnimalsApoptosisColitisDextran SulfateHumansInflammationLymphocytesMaleMiceMice, Inbred C57BLTumor Suppressor Protein p53Dextran SulfateTumor Suppressor Protein p53

Identifiers

PMID20179294
PMCPMC2833220
OpenAlexW2137234764

What OpenQuestion holds

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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.