Evidence map›Paper›PMID 26714752›Full record

ArticleIn vitro cellular & developmental biology. Animal2016

Ginsenoside Rg5:Rk1 attenuates TNF-α/IFN-γ-induced production of thymus- and activation-regulated chemokine (TARC/CCL17) and LPS-induced NO production via downregulation of NF-κB/p38 MAPK/STAT1 signaling in human keratinocytes and macrophages.

Sungeun Ahn, Muhammad Hanif Siddiqi, Veronica Castro Aceituno, Shakina Yesmin Simu, Jinglou Zhang, Zuly Elizabeth Jimenez Perez, Yu-Jin Kim, Deok-Chun Yang

Abstract read
PubMed Publisher
In one paragraph

Article in In vitro cellular & developmental biology. Animal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
10.4field-weighted citation impact, top 1% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
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  16. Effects ofHeliyon · 2023
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  18. Pharmaceuticals (Basel, Switzerland) · 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

8 authors at 1 institution in 1 country.

Sungeun AhnDepartment of Oriental Medicinal Biotechnology, College of Life Sciences, Kyung Hee University, Yongin, 446-701, Republic of Korea.
Muhammad Hanif SiddiqiGinseng Bank, Graduate School of Biotechnology, College of Life Sciences, Kyung Hee University, Yongin, 446-701, Republic of Korea.
Veronica Castro AceitunoDepartment of Oriental Medicinal Biotechnology, College of Life Sciences, Kyung Hee University, Yongin, 446-701, Republic of Korea.
Shakina Yesmin SimuGinseng Bank, Graduate School of Biotechnology, College of Life Sciences, Kyung Hee University, Yongin, 446-701, Republic of Korea.
Jinglou ZhangGinseng Bank, Graduate School of Biotechnology, College of Life Sciences, Kyung Hee University, Yongin, 446-701, Republic of Korea.
Zuly Elizabeth Jimenez PerezGinseng Bank, Graduate School of Biotechnology, College of Life Sciences, Kyung Hee University, Yongin, 446-701, Republic of Korea.
Yu-Jin KimDepartment of Oriental Medicinal Biotechnology, College of Life Sciences, Kyung Hee University, Yongin, 446-701, Republic of Korea.
Deok-Chun YangDepartment of Oriental Medicinal Biotechnology, College of Life Sciences, Kyung Hee University, Yongin, 446-701, Republic of Korea. yangdeokchun@gmail.com.
Kyung Hee University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atopic dermatitis (AD) is a chronic skin disease that affects millions of people worldwide. Keratinocytes and macrophages are two cells types that play a pivotal role in the development of AD. These cells produced different chemokines and cytokines, especially thymus and activation-regulated chemokine (TARC/CCL17) and macrophage-derived chemokine (MDC/CCL22), as well as nitric oxide (NO) through inducible nitric oxide synthase (iNOS) and COX2 in response to stimulation by TNF-α/IFN-γ and lipopolysaccharide (LPS) respectively. These mediators are thought to be crucial regulators of the pathogenesis of AD. Although several natural compounds to treat AD have been studied, the effect of Rg5:Rk1 from Panax ginseng (P. ginseng) on AD has not yet been investigated. In this study, we evaluated the inhibitory effect of Rg5:Rk1 on TNF-α/IFN-γ stimulated keratinocytes (HaCaT cells) and LPS-stimulated macrophages (RAW 264.7 cells). Enzyme-linked immunosorbent assay (ELISA) data showed that pretreatment of HaCaT cells with Rg5:Rk1 significantly reduced the TNF-α/IFN-γ-induced increase in TARC/CCL17 expression in a dose-dependent manner. In addition, Rg5:Rk1 decreased LPS-mediated nitric oxide (NO) and reactive oxygen species (ROS) production in RAW 264.7 cells. A considerable reduction in messenger RNA (mRNA) expression of the aforementioned AD mediators was also observed. Pretreatment with Rg5:Rk1 attenuated the TNF-α/IFN-γ-induced phosphorylation of p38 MAPK, STAT1, and NF-κB/IKKβ in HaCaT cells. Together, these findings suggest that ginsenoside Rg5:Rk1 may have a potential anti-AD effect by suppressing NF-κB/p38 MAPK/STAT1 signaling.

Indexed as

AnimalsCell LineChemokine CCL17Chemokine CCL22Dermatitis, AtopicDown-RegulationGinsenosidesHumansI-kappa B KinaseInterferon-gammaKeratinocytesLipopolysaccharidesMacrophagesMiceNitric Oxidep38 Mitogen-Activated Protein KinasesCCL22 protein, humanChemokine CCL17Chemokine CCL22ginsenoside Rg5GinsenosidesI-kappa B KinaseInterferon-gammaLipopolysaccharidesNitric Oxidep38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesRELA protein, humanSTAT1 protein, humanSTAT1 Transcription FactorTranscription Factor RelATumor Necrosis Factor-alphaAtopic dermatitisInflammationKeratinocytes/macrophages TARC/CCL17NF-κBp38 MAPKSTAT1

Identifiers

PMID26714752
OpenAlexW2204154222

What OpenQuestion holds

Textmetadata
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.