Evidence map›Paper›PMID 25535478›Full record

ArticleJournal of ginseng research2015

Molecular mechanism of protopanaxadiol saponin fraction-mediated anti-inflammatory actions.

Yanyan Yang, Jongsung Lee, Man Hee Rhee, Tao Yu, Kwang-Soo Baek, Nak Yoon Sung, Yong Kim, Keejung Yoon, Ji Hye Kim, Yi-Seong Kwak and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of ginseng research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 74 citations in OpenAlex.

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  19. AKT-targeted anti-inflammatory activity ofJournal of ginseng research · 2018
    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

13 authors at 4 institutions in 1 country.

Yanyan YangDepartment of Genetic Engineering, Sungkyunkwan University, Suwon, Korea.
Jongsung LeeDepartment of Dermatological Health Management, Eulji University, Seongnam, Korea.
Man Hee RheeCollege of Veterinary Medicine, Kyungpook National University, Daegu, Korea.
Tao YuDepartment of Genetic Engineering, Sungkyunkwan University, Suwon, Korea.
Kwang-Soo BaekDepartment of Genetic Engineering, Sungkyunkwan University, Suwon, Korea.
Nak Yoon SungDepartment of Genetic Engineering, Sungkyunkwan University, Suwon, Korea.
Yong KimDepartment of Genetic Engineering, Sungkyunkwan University, Suwon, Korea.
Keejung YoonDepartment of Genetic Engineering, Sungkyunkwan University, Suwon, Korea.
Ji Hye KimDepartment of Genetic Engineering, Sungkyunkwan University, Suwon, Korea.
Yi-Seong KwakGinseng Corporation Central Research Institute, Daejeon, Korea.
Sungyoul HongDepartment of Genetic Engineering, Sungkyunkwan University, Suwon, Korea.
Jong-Hoon KimDepartment of Veterinary Physiology, College of Veterinary Medicine, Biosafety Research Institute, Chonbuk National University, Jeonju, Korea.
Jae Youl ChoDepartment of Genetic Engineering, Sungkyunkwan University, Suwon, Korea.
Sungkyunkwan University · KRJeonbuk National University · KREulji University · KRKyungpook National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKorean Red Ginseng (KRG) is a representative traditional herbal medicine with many different pharmacological properties including anticancer, anti-atherosclerosis, anti-diabetes, and anti-inflammatory activities. Only a few studies have explored the molecular mechanism of KRG-mediated anti-inflammatory activity.

methodsWe investigated the anti-inflammatory mechanisms of the protopanaxadiol saponin fraction (PPD-SF) of KRG using in vitro and in vivo inflammatory models.

resultsPPD-SF dose-dependently diminished the release of inflammatory mediators [nitric oxide (NO), tumor necrosis factor-α, and prostaglandin E2], and downregulated the mRNA expression of their corresponding genes (inducible NO synthase, tumor necrosis factor-α, and cyclooxygenase-2), without altering cell viability. The PPD-SF-mediated suppression of these events appeared to be regulated by a blockade of p38, c-Jun N-terminal kinase (JNK), and TANK (TRAF family member-associated NF-kappa-B activator)-binding kinase 1 (TBK1), which are linked to the activation of activating transcription factor 2 (ATF2) and interferon regulatory transcription factor 3 (IRF3). Moreover, this fraction also ameliorated HCl/ethanol/-induced gastritis via suppression of phospho-JNK2 levels.

conclusionThese results strongly suggest that the anti-inflammatory action of PPD-SF could be mediated by a reduction in the activation of p38-, JNK2-, and TANK-binding-kinase-1-linked pathways and their corresponding transcription factors (ATF2 and IRF3).

Indexed as

activating transcription factor 2anti-inflammatory activityinterferon regulatory transcription factor 3Korean red ginsengprotopanaxadiol saponin fraction

Identifiers

PMID25535478
PMCPMC4268567
OpenAlexW2109164884

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.