Evidence map›Paper›PMID 38125068›Full record

ArticleArchives of rheumatology2023

GCSB-5 regulates inflammatory arthritis and pain by modulating the mitogen-activated protein kinase signaling pathway in a murine model of rheumatoid arthritis.

Jihye Bang, Gyeonghwa Kim, Soo Young Park, Hye Ra Jung, Sang-Hyon Kim, Ji-Min Kim

Open access · diamondAbstract read
In one paragraph

Article in Archives of rheumatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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

6 authors at 3 institutions in 1 country.

Jihye BangDepartment of Chronic Disease Convergence Research, Division of Allergy and Respiratory Disease Research, Korea National Institute of Health, Korea Disease Control and Prevention Agency, Cheongju, South Korea.ORCID 0000-0002-9343-4646
Gyeonghwa KimDivision of Rheumatology, Department of Internal Medicine, School of Medicine & Institute for Medical Science, Keimyung University, Daegu, South Korea.ORCID 0000-0002-3795-4735
Soo Young ParkDepartment of Internal Medicine,School of Medicine, Kyungpook National University, Kyungpook National University Hospital, Daegu, South Korea.ORCID 0000-0002-4944-4396
Hye Ra JungDepartment of Pathology, Keimyung University School of Medicine, Daegu, South Korea.ORCID 0000-0002-1477-6606
Sang-Hyon KimDivision of Rheumatology, Department of Internal Medicine, School of Medicine & Institute for Medical Science, Keimyung University, Daegu, South Korea.ORCID 0000-0002-8030-7939
Ji-Min KimDivision of Rheumatology, Department of Internal Medicine, School of Medicine & Institute for Medical Science, Keimyung University, Daegu, South Korea.ORCID 0000-0002-3894-3413
Keimyung University · KRKorea Disease Control and Prevention Agency · KRKyungpook National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: This study aimed to determine whether GCSB-5 has anti-inflammatory and antinociceptive effects in mice with collagen-induced arthritis (CIA), an animal model of rheumatoid arthritis (RA), and investigate the influence of GCSB-5 on the mitogen-activated protein kinase (MAPK) pathway. Materials and methods: The experimental animal study was designed to include five groups: CIA mice treated with GCSB-5 (300 mg/kg), GCSB-5 (600 mg/kg), celecoxib (60 mg/kg), or saline for four weeks, and nontreated control mice. The clinical severity of arthritis was scored. Nociceptive thresholds were measured by using a von Frey dynamic plantar analgesimeter. The MAPK pathway was evaluated in mouse synovium. The expression of channels associated with pain signaling was assessed by western blot and immunohistochemical staining. Results: GCSB-5 treatment diminished the severity of clinical arthritis and increased the nociceptive threshold in mice with CIA. Celecoxib, a positive control drug, also showed comparable changes. Clinical arthritis scores were inversely related to mechanical thresholds. GCSB-5 administration decreased the levels of anti-type II collagen antibody and inflammatory cytokines in the sera of mice with CIA. Furthermore, ERK, p38 MAPK, and JNK phosphorylation were downregulated and TRPV1 and ASIC3 expression were decreased in the synovium of GCSB-5-treated mice compared to salinetreated mice. Interleukin-6-induced TRPV1 and ASIC3 upregulation were also inhibited by GCSB-5 in human RA fibroblast-like synoviocytes Conclusion: GCSB-5 decreased inflammatory arthritis and pain in a murine model of RA. The results present evidence that GCSB-5 may be beneficial for relieving pain as well as decreasing inflammation in autoimmune arthritis, such as RA.

Indexed as

Anti-inflammatory agentsASIC3plant extractsrheumatoid arthritisTRPV1.

Identifiers

PMID38125068
PMCPMC10728744
OpenAlexW4389338695

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Registered trials

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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.