Evidence map›Paper›PMID 37809903›Full record

ArticleHeliyon2023

Methyl lucidone inhibits airway inflammatory response by reducing TAK1 activity in human bronchial epithelial NCI-H292 cells.

Eun Sol Oh, Hyunju Ro, Hyung Won Ryu, Yu Na Song, Ji-Yoon Park, Namho Kim, Hae-Young Kim, Seon Min Oh, Su-Yeon Lee, Doo-Young Kim and 4 more

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.0field-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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

14 authors at 2 institutions in 1 country.

Eun Sol OhNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea.
Hyunju RoDepartment of Biological Sciences, College of Bioscience and Biotechnology, Chungnam National University, Daejeon, 34134, Republic of Korea.
Hyung Won RyuNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea.
Yu Na SongNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea.
Ji-Yoon ParkNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea.
Namho KimNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea.
Hae-Young KimNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea.
Seon Min OhNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea.
Su-Yeon LeeNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea.
Doo-Young KimNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea.
Sooil KimDepartment of Anatomy and Cell Biology, Department of Medical Science, College of Medicine, Chungnam National University, Daejeon, 35015, Republic of Korea.
Sung-Tae HongDepartment of Anatomy and Cell Biology, Department of Medical Science, College of Medicine, Chungnam National University, Daejeon, 35015, Republic of Korea.
Mun-Ock KimNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea.
Su Ui LeeNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea.
Chungnam National University · KRKorea Research Institute of Bioscience and Biotechnology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Methyl lucidone (ML), a methyl derivative of lucidone, has anti-inflammatory properties. However, the molecular mechanisms that reduce the inflammatory effect of ML in human lung epithelial cells remain unkown. This study aimed to elucidate the molecular mechanisms underlying the anti-inflammatory effect of ML. Methods: Four compounds (ML, methyl linderone, kanakugiol, and linderone) from Results: ML treatment effectively reduced the levels of inflammatory cytokines, including interleukin-1β and TNF-α, increased by stimulation. Furthermore, ML downregulated the pathway cascade of both IκB kinase (IKK)/NF-κB and p38 mitogen-activated protein (MAP) kinase/CREB by inhibiting the upstream kinase TAK1. An Conclusion: ML pretreatment repressed the PMA-stimulated inflammation reaction by reducing the TAK1-mediated IKK/NF-κB and p38 MAP kinase/CREB signaling. These findings suggest that ML may improve respiratory health and can be used as a dietary supplement or functional food to prevent inflammatory lung diseases.

Indexed as

Human bronchial epithelial cellInflammatory lung diseaseMethyl lucidoneNF-κBp38 MAP kinaseTAK1

Identifiers

PMID37809903
PMCPMC10559928
OpenAlexW4386797322

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.