Evidence map›Paper›PMID 39639498›Full record

ArticleJournal of microbiology and biotechnology2024

Aromadendrin Ameliorates Airway Inflammation in Experimental Mice with Chronic Obstructive Pulmonary Disease.

Jinseon Choi, Seok Han Yun, Hyueyun Kim, Juhyun Lee, Seong-Man Kim, Mi-Hyeong Park, Hee Jae Lee, Wanjoo Chun, Sang-Bae Han, Kyung-Seop Ahn and 1 more

Abstract read
In one paragraph

Article in Journal of microbiology and biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Jinseon ChoiNatural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju 28116, Republic of Korea.
Seok Han YunNatural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju 28116, Republic of Korea.
Hyueyun KimNatural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju 28116, Republic of Korea.
Juhyun LeeNatural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju 28116, Republic of Korea.
Seong-Man KimO2MEDi Inc. 50 UNIST-gil, Eonyang-eup, Ulju-gun, Ulsan 44919, Republic of Korea.
Mi-Hyeong ParkOffice of Surveillance for Narcotics Abuse, Ministry of Food and Drug Safety, Osong Health Technology Administration Complex, Cheongju 28159, Republic of Korea.
Hee Jae LeeDepartment of Pharmacology, College of Medicine, Kangwon National University, Chuncheon 24341, Republic of Korea.
Wanjoo ChunDepartment of Pharmacology, College of Medicine, Kangwon National University, Chuncheon 24341, Republic of Korea.
Sang-Bae HanCollege of Pharmacy, Chungbuk National University, Cheongju 28160, Republic of Korea.
Kyung-Seop AhnNatural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju 28116, Republic of Korea.
Jae-Won LeeNatural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju 28116, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aromadendrin (ARO) is an active plant compound that exerts anti-inflammatory effects. However, its ameliorative effects on chronic obstructive pulmonary disease (COPD) remain unclear. Therefore, we investigated the inhibitory effects of ARO on bronchial inflammation using an experimental model of COPD. In vivo analysis confirmed a notable increase in the number of neutrophils/macrophages and the formation of reactive oxygen species (ROS), myeloperoxidase (MPO), interleukin (IL)-6/IL-1β, and monocyte chemoattractant protein (MCP)-1 in the bronchoalveolar lavage (BAL) fluid of COPD mice, which was attenuated by oral gavage of ARO. In addition, hematoxylin and eosin staining showed a notable cell influx in the lungs of the COPD group, which was ameliorated by ARO. Western blotting revealed that ARO decreased the upregulation of neutrophil elastase expression in the lungs of the COPD group. Furthermore, periodic acid-Schiff staining showed that increased mucus formation in the lungs of the COPD group was downregulated by ARO. ARO also blocked CREB activation in the lungs of COPD mice. This in vivo, anti-inflammatory effect of ARO was accompanied by its modulatory effect on the activation of the MAPK/NF-κB/NLRP3 inflammasome. In summary, our study demonstrated that ARO has protective effects on bronchial inflammation by attenuating immune cell accumulation, toxic molecule/cytokine/chemokine formation, and MAPK/NF-κB/NLRP3 inflammasome activation, suggesting the potential development of ARO as an adjuvant for the prevention and treatment of COPD.

Indexed as

Anti-Inflammatory AgentsInflammationPulmonary Disease, Chronic ObstructiveAnimalsBronchoalveolar Lavage FluidCytokinesDisease Models, AnimalInflammasomesLungMacrophagesMaleMiceMice, Inbred C57BLNeutrophilsNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinAnti-Inflammatory AgentsCytokinesInflammasomesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinPeroxidaseReactive Oxygen SpeciesaromadendrinCOPDcytokinesNF-κBNLRP3 inflammasome

Identifiers

PMID39639498
PMCPMC11813338

What Socratic holds

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LicenceCC BY
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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 Socratic graph.