Evidence map›Paper›PMID 31817146›Full record

ArticleInternational journal of molecular sciences2019

Ginsenoside Rh2 Ameliorates Atopic Dermatitis in NC/Nga Mice by Suppressing NF-kappaB-Mediated Thymic Stromal Lymphopoietin Expression and T Helper Type 2 Differentiation.

Eunsu Ko, Sungjoo Park, Jun Hyoung Lee, Chang-Hao Cui, Jingang Hou, Myung-Ho Kim, Sun Chang Kim

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

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

  1. Pooled it
  2. Study on the Therapeutic Effects of Ginsenoside Rh2 in Asthma Improvement.International journal of molecular sciences · 2026
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  14. Frontiers in pharmacology · 2022
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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

7 authors at 2 institutions in 1 country.

Eunsu KoDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 34141, Korea.
Sungjoo ParkDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 34141, Korea.
Jun Hyoung LeeDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 34141, Korea.
Chang-Hao CuiIntelligent Synthetic Biology Center, Daejeon 34141, Korea.
Jingang HouIntelligent Synthetic Biology Center, Daejeon 34141, Korea.
Myung-Ho KimLaboratory of Liver Research, Graduate School of Medical Science and Engineering, KAIST, Daejeon 34141, Korea.
Sun Chang KimDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 34141, Korea.
Korea Advanced Institute of Science and Technology · KRIntelligent Synthetic Biology Center · KR

Funding

Ministry of Science ICT and Future Planning 2011-0031955
6 · The paper itself

Abstract

Ginsenosides are known to have various highly pharmacological activities, such as anti-cancer and anti-inflammatory effects. However, the search for the most effective ginsenosides against the pathogenesis of atopic dermatitis (AD) and the study of the effects of ginsenosides on specific cytokines involved in AD remain unclear. In this study, ginsenoside Rh2 was shown to exert the most effective anti-inflammatory action on thymic stromal lymphopoietin (TSLP) and interleukin 8 in tumor necrosis factor-alpha and polyinosinic: polycytidylic acid induced normal human keratinocytes by inhibiting proinflammatory cytokines at both protein and transcriptional levels. Concomitantly, Rh2 also efficiently alleviated 2,4-dinitrochlorobenzene-induced AD-like skin symptoms when applied topically, including suppression of immune cell infiltration, cytokine expression, and serum immunoglobulin E levels in NC/Nga mice. In line with the in vitro results, Rh2 inhibited TSLP levels in AD mice via regulation of an underlying mechanism involving the nuclear factor κB pathways. In addition, in regard to immune cells, we showed that Rh2 suppressed not only the expression of TSLP but the differentiation of naïve CD4+ T-cells into T helper type 2 cells and their effector function in vitro. Collectively, our results indicated that Rh2 might be considered as a good therapeutic candidate for the alternative treatment of AD.

Indexed as

AnimalsCD4-Positive T-LymphocytesCell DifferentiationCell LineCytokinesDermatitis, AtopicDinitrochlorobenzeneDisease Models, AnimalDown-RegulationGinsenosidesHumansImmunoglobulin EMaleMiceNF-kappa BSkinCytokinesDinitrochlorobenzeneginsenoside Rh2GinsenosidesImmunoglobulin ENF-kappa BThymic Stromal Lymphopoietinatopic dermatitisginsengginsenosideNF-κB pathwayTh2 differentiationthymic stromal lymphopoietin

Identifiers

PMID31817146
PMCPMC6940811
OpenAlexW2991757916

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.