Evidence map›Paper›PMID 38281189›Full record

ArticleMolecular biology reports2024

Cardamonin decreases inflammatory mediator expression in IL-1β-stimulated human periodontal ligament cells.

Risa Okamoto, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Keiichi Hosaka

Abstract read
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In one paragraph

Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. 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

5 authors at 1 institution in 1 country.

Risa OkamotoDepartment of Regenerative Dental Medicine, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto-cho, Tokushima, Tokushima, 770-8504, Japan.
Yoshitaka HosokawaDepartment of Regenerative Dental Medicine, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto-cho, Tokushima, Tokushima, 770-8504, Japan. hosokawa@tokushima-u.ac.jp.
Ikuko HosokawaDepartment of Regenerative Dental Medicine, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto-cho, Tokushima, Tokushima, 770-8504, Japan.
Kazumi OzakiDepartment of Oral Health Care Promotion, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Tokushima, Japan.
Keiichi HosakaDepartment of Regenerative Dental Medicine, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto-cho, Tokushima, Tokushima, 770-8504, Japan.
Tokushima University · JP

Funding

Cluster program of Tokushima University 2202006Japan Society for the Promotion of Science 22K09966 and 22K09984
6 · The paper itself

Abstract

backgroundCardamonin is classified as a natural chalcone, and has been reported to possess various bioactive effects. However, there have been limited attempts to utilize cardamonin in the treatment of periodontitis. This study aimed to investigate whether cardamonin has anti-inflammatory effects on human periodontal ligament cells (HPDLCs), which are a component cell of periodontal tissue. Specifically, the study seeks to determine whether cardamonin affects the expression of inflammatory mediators, such as cytokines and adhesion molecules, induced by interleukin-1β (IL-1β) in HPDLCs, as well as the signaling pathways activated by IL-1β.

methodsCytokine and chemokine levels in supernatants of HPDLCs were measured by ELISA. Western blot analysis was used to measure protein expression and signal transduction pathway activation in HPDLCs.

resultsWe found that IL-1β-induced CC chemokine ligand (CCL)2, CCL5, CCL20, CXC-chemokine ligand (CXCL)10, and interleukin (IL)-6 production and intercellular adhesion molecule (ICAM)-1 and cyclooxygenase (COX)-2 expression in HPDLCs were suppressed by cardamonin treatment. We also found that cardamonin suppressed IL-1β-activated nuclear factor (NF)-κB pathway, and the phosphorylation of signal transducer and activator of transcription (STAT)3. Furthermore, cardamonin treatment enhanced the expression of the antioxidant enzymes, heme oxygenase (HO)-1 and NAD(P)H dehydrogenase [quinone] 1 (NQO1), in HPDLCs.

conclusionIn this study, we found that cardamonin could suppress the production of inflammatory mediators in HPDLCs as well as the activation of several signaling pathways induced by IL-1β treatment.

Indexed as

ChalconesCells, CulturedChemokinesCyclooxygenase 2CytokinesHumansInflammation MediatorsInterleukin-1betaLigandsNF-kappa BPeriodontal LigamentcardamoninChalconesChemokinesCyclooxygenase 2CytokinesInflammation MediatorsInterleukin-1betaLigandsNF-kappa BAnti-inflammatory effectAntioxidant enzymeCardamoninPeriodontal ligament cellsSignal transduction

Identifiers

PMID38281189
OpenAlexW4391298040

What OpenQuestion holds

Textmetadata
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.