Evidence map›Paper›PMID 37559380›Full record

ArticlePharmaceutical biology2023

Glucocorticoid receptors involved in ginsenoside compound K ameliorate adjuvant arthritis by inhibiting the glycolysis of fibroblast-like synoviocytes via the NF-κB/HIF-1α pathway.

Yating Wang, Xiurong Bao, Hao Xian, Fang Wei, Yining Song, Siyu Zhao, Yujie Zhang, Yumeng Wang, Ying Wang

Open access · goldAbstract read
In one paragraph

Article in Pharmaceutical biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Yating WangSchool of Pharmacy, Bengbu Medical College, Bengbu, Anhui, P.R. China.
Xiurong BaoSchool of Pharmacy, Bengbu Medical College, Bengbu, Anhui, P.R. China.
Hao XianSchool of Pharmacy, Bengbu Medical College, Bengbu, Anhui, P.R. China.
Fang WeiSchool of Pharmacy, Bengbu Medical College, Bengbu, Anhui, P.R. China.
Yining SongSchool of Pharmacy, Bengbu Medical College, Bengbu, Anhui, P.R. China.
Siyu ZhaoSchool of Pharmacy, Bengbu Medical College, Bengbu, Anhui, P.R. China.
Yujie ZhangSchool of Pharmacy, Bengbu Medical College, Bengbu, Anhui, P.R. China.
Yumeng WangSchool of Pharmacy, Bengbu Medical College, Bengbu, Anhui, P.R. China.
Ying WangSchool of Pharmacy, Bengbu Medical College, Bengbu, Anhui, P.R. China.
Bengbu Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextGinsenoside metabolite compound K (CK) is an active metabolite produced by ginsenosides

objectiveThis study explores the role and potential mechanisms of CK MATERIALS AND

methodsAdjuvant arthritis (AA) model was induced in Sprague-Dawley (SD) rats; the rats were randomly divided into four groups (

resultsCK (80 mg/kg) reduced paw swelling (52%) and arthritis global assessment (31%) compared to that in AA rats. In addition, CK (80 mg/kg) suppressed GLUT1 (38%), HK2 (50%), and PKM2 (56%) levels compared with those in AA FLS. However, the effects of CK (30 μM) on these events were weakened or enhanced after GR knockdown or overexpression in FLS stimulated by TNF-α (30 ng/mL). CK (80 mg/kg) also downregulated the expression of P65 (61%), p-IκB (92%), and HIF-1α (59%). DISCUSSION AND

conclusionsThe inhibition of CK on glycolysis and the NF-κB/HIF-1α pathway is potentially mediated through activating GR. These findings provide experimental evidence for elucidating the molecular mechanism of CK in treating rheumatoid arthritis (RA).

Indexed as

Arthritis, ExperimentalGinsenosidesSynoviocytesAnimalsCell ProliferationFibroblastsGlycolysisNF-kappa BRatsRats, Sprague-DawleyReceptors, GlucocorticoidSynovial MembraneTumor Necrosis Factor-alphaginsenoside compound KGinsenosidesNF-kappa BReceptors, GlucocorticoidTumor Necrosis Factor-alphahypoxia-inducible factor-1αInflammationnuclear factor κB

Identifiers

PMID37559380
PMCPMC10416744
OpenAlexW4385715266

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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.