Evidence map›Paper›PMID 31835494›Full record

ArticleMolecules (Basel, Switzerland)2019

Taurochenodeoxycholic Acid Inhibited AP-1 Activation via Stimulating Glucocorticoid Receptor.

Lei Li, Chang Liu, Wei Mao, Bayaer Tumen, Peifeng Li

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. DietaryFrontiers in veterinary science · 2026
    Article
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  5. Review
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  11. Frontiers in nutrition · 2022
    Article
  12. Review
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  14. Article
  15. Cell-specific expression ofInternational journal of immunopathology and pharmacology
    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

5 authors at 3 institutions in 1 country.

Lei LiKey Laboratory of Quality & Safety Control for Pork, Ministry of Agriculture and Rural, College of Animal Science, Anhui Science and Technology University, Fengyang 233100, China.ORCID 0000-0002-1670-6599
Chang LiuKey Laboratory of Quality & Safety Control for Pork, Ministry of Agriculture and Rural, College of Animal Science, Anhui Science and Technology University, Fengyang 233100, China.ORCID 0000-0002-1092-0762
Wei MaoKey Laboratory of Clinical Diagnosis and Treatment Techniques for Animal Disease, Ministry of Agriculture and Rural, College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot 010018, China.
Bayaer TumenShanxi Animal Disease Control Center, Taiyuan 030027, China.
Peifeng LiKey Laboratory of Clinical Diagnosis and Treatment Techniques for Animal Disease, Ministry of Agriculture and Rural, College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot 010018, China.
Anhui University of Science and Technology · CNInner Mongolia Agricultural University · CNChina Animal Disease Control Center · CN

Funding

Leading Academic Discipline Project of Anhui Science and Technology University AKZDXK2015A04Natural Science Key Foundation of Anhui Education Department KJ2017A503, KJ2017A504Talent Project of Anhui Science and Technology University ZRC2014447the National Natural Science Foundation of China 31160518, 31272605, 31802242Young Talents Visiting and Training Program for Foreign Country gxgwfx2019047
6 · The paper itself

Abstract

Taurochenodeoxycholic acid (TCDCA) as a primary bioactive substance of animal bile has been shown to exert good anti-inflammatory and immunomodulatory functions in adjuvant arthritis in rats. The anti-inflammatory and immunomodulatory properties of TCDCA have exhibited interesting similarities with the effects of glucocorticoids (GCs). To investigate the potential mechanisms of TCDCA in anti-inflammation and immunomodulation, we used a luciferase reporter assay to evaluate the activation of the glucocorticoid receptor (GR) stimulated by TCDCA. Our results showed that GR was activated by TCDCA in a concentration-dependent manner. Moreover, the elevated expressions of c-Fos and phosphorylated c-Jun induced by interleukin-1β (IL-1β) were reversed by TCDCA. The inhibition of TCDCA on the transactivation of activator protein-1 (AP-1) was observed as well. However, the suppression of TCDCA on the phosphorylation of c-Jun was blocked incompletely by GR inhibitor RU486. These results have indicated that the anti-inflammatory and immunomodulatory functions of TCDCA involve multiple pathways, with contributions from GR and its related AP-1 signaling pathway.

Indexed as

AnimalsCell SurvivalMaleMolecular StructurePhosphorylationProtein BindingProto-Oncogene Proteins c-fosRatsReceptors, GlucocorticoidTaurochenodeoxycholic AcidTranscriptional ActivationTranscription Factor AP-1Proto-Oncogene Proteins c-fosReceptors, GlucocorticoidTaurochenodeoxycholic AcidTranscription Factor AP-1activator protein-1anti-inflammationglucocorticoid receptortaurochenodeoxycholic acid

Identifiers

PMID31835494
PMCPMC6943563
OpenAlexW2996576959

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.