Evidence map›Paper›PMID 34764724›Full record

ArticleJournal of ginseng research2021

Ginsenoside F1 Attenuates Eosinophilic Inflammation in Chronic Rhinosinusitis by Promoting NK Cell Function.

So Jeong Kim, Jinju Lee, Woo Sun Choi, Hyo Jeong Kim, Mi-Yeon Kim, Sun Chang Kim, Hun Sik Kim

Open access · goldAbstract read
In one paragraph

Article in Journal of ginseng research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Therapeutic Applications of Ginseng Natural Compounds for Health Management.International journal of molecular sciences · 2023
    Review
  6. Inhibitory Effects ofPlants (Basel, Switzerland) · 2022
    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

7 authors at 1 institution in 1 country.

So Jeong KimDepartment of Biomedical Sciences, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Jinju LeeDepartment of Biomedical Sciences, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Woo Sun ChoiDepartment of Biomedical Sciences, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Hyo Jeong KimDepartment of Biomedical Sciences, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Mi-Yeon KimDepartment of Biomedical Sciences, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Sun Chang KimDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.
Hun Sik KimDepartment of Biomedical Sciences, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Ulsan College · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGinsenosides have beneficial effects on several airway inflammatory disorders primarily through glucocorticosteroid-like anti-inflammatory activity. Among inflammatory cells, eosinophils play a major pathogenic role in conferring a risk of severe refractory diseases including chronic rhinosinusitis (CRS). However, the role of ginsenosides in reducing eosinophilic inflammation and CRS pathogenesis is unexplored.

methodsWe investigated the therapeutic efficacy and underlying mechanism of ginsenoside F1 (G-F1) in comparison with those of dexamethasone, a representative glucocorticosteroid, in a murine model of CRS. The effects of G-F1 or dexamethasone on sinonasal abnormalities and infiltration of eosinophils and mast cells were evaluated by histological analyses. The changes in inflammatory cytokine levels in sinonasal tissues, macrophages, and NK cells were assessed by qPCR, ELISA, and immunohistochemistry.

resultsWe found that G-F1 significantly attenuated eosinophilic inflammation, mast cell infiltration, epithelial hyperplasia, and mucosal thickening in the sinonasal mucosa of CRS mice. Moreover, G-F1 reduced the expression of IL-4 and IL-13, as well as hematopoietic prostaglandin D synthase required for prostaglandin D

conclusionOur results suggest that potentiating NK cell activity, for example with G-F1, is a promising strategy for resolving eosinophilic inflammation in CRS.

Indexed as

CRSdexamethasoneeosinophilG-F1NK cell

Identifiers

PMID34764724
PMCPMC8569323
OpenAlexW3141092905

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.