Evidence map›Paper›PMID 31936879›Full record

ArticleBiomolecules2020

A Critical Regulation of Th17 Cell Responses and Autoimmune Neuro-Inflammation by Ginsenoside Rg3.

Young-Jun Park, Minkyoung Cho, Garam Choi, Hyeongjin Na, Yeonseok Chung

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Recent trends in ginseng research.Journal of natural medicines · 2024
    Review
  3. Review
  4. Anti-leukemia effects of ginsenoside monomer: A narrative review of pharmacodynamics study.Current therapeutic research, clinical and experimental · 2024
    Review
  5. Review
  6. Article
  7. The "Treatise on the spleen and stomach" (Journal of traditional and complementary medicine · 2020
    Review
  8. Advances in Ginsenosides.Biomolecules · 2020
    Article
  9. 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

5 authors at 1 institution in 1 country.

Young-Jun ParkLaboratory of Immune Regulation, Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 08826, Korea.
Minkyoung ChoLaboratory of Immune Regulation, Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 08826, Korea.
Garam ChoiLaboratory of Immune Regulation, Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 08826, Korea.
Hyeongjin NaLaboratory of Immune Regulation, Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 08826, Korea.
Yeonseok ChungLaboratory of Immune Regulation, Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 08826, Korea.
Seoul National University · KR

Funding

Korean Society of Ginseng Korean Society of Ginseng
6 · The paper itself

Abstract

Among diverse helper T-cell subsets, Th17 cells appear to be pathogenic in diverse autoimmune diseases, and thus, targeting Th17 cells could be beneficial for the treatment of the diseases in humans. Ginsenoside Rg3 is one of the most potent components in Korean Red Ginseng (KRG;

Indexed as

AnimalsAnti-Inflammatory AgentsCells, CulturedEncephalomyelitis, Autoimmune, ExperimentalFemaleGinsenosidesInflammationMice, Inbred C57BLTh17 CellsAnti-Inflammatory Agentsginsenoside Rg3GinsenosidesEAERg3RORγtTh17

Identifiers

PMID31936879
PMCPMC7023269
OpenAlexW3000336288

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.