Evidence map›Paper›PMID 39757204›Full record

ArticleBMB reports2025

Quantum molecular resonance ameliorates atopic dermatitis through suppression of IL36G and SPRR2B.

Jinyoung Kim, Barsha Deshar, Min Hwang, Chandani Shrestha, Eunhye Ju, Bum-Ho Bin, Jiyoon Kim

Abstract read
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In one paragraph

Article in BMB reports, 2025. 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
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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.

  1. Article
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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

7 authors.

Jinyoung KimDepartment of Pharmacology, College of Medicine, The Catholic University of Korea, Seoul 06591; Department of Medical Sciences, Graduate School, The Catholic University of Korea, Seoul 06591, Korea.
Barsha DesharDepartment of Pharmacology, College of Medicine, The Catholic University of Korea, Seoul 06591; Department of Medical Sciences, Graduate School, The Catholic University of Korea, Seoul 06591, Korea.
Min HwangDepartment of Pharmacology, College of Medicine, The Catholic University of Korea, Seoul 06591; Department of Medical Sciences, Graduate School, The Catholic University of Korea, Seoul 06591, Korea.
Chandani ShresthaDepartment of Pharmacology, College of Medicine, The Catholic University of Korea, Seoul 06591; Department of Medical Sciences, Graduate School, The Catholic University of Korea, Seoul 06591, Korea.
Eunhye Juwho clinic, Incheon 21395, Korea.
Bum-Ho BinDepartment of Applied Biotechnology, Ajou University, Suwon 16499; Department of Biological Sciences, Ajou University, Suwon 16499, Korea.
Jiyoon KimDepartment of Pharmacology, College of Medicine, The Catholic University of Korea, Seoul 06591; Department of Medical Sciences, Graduate School, The Catholic University of Korea, Seoul 06591; Institute for Aging and Metabolic Diseases, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atopic dermatitis (AD) is a chronic, pruritic skin disease characterized by inflammation and skin lesion cornification. While the use of corticosteroids like dexamethasone (DXM), an antiinflammatory drug, improves symptoms temporarily and quickly, this use is not a cure. Thus, we aimed to identify a new therapeutic strategy for AD using quantum molecular resonance (QMR), a novel non-invasive technique with an electromagnetic field-based therapeutic approach as an alternative to pain killers. An AD mouse model presenting AD-like skin lesions was generated by treating BALB/c mice with dinitrochlorobenzene (DNCB), and then DNCB-induced AD mice were administered DXM or QMR, and the change of AD-like skin lesions was observed. QMR ameliorated AD-like skin lesions in DNCB-induced AD mice and reduced the numbers of infiltrated mast cells and macrophages in mouse skin. QMR also alleviated thickening of the epidermis and restored integrity of the epidermal basement membrane. Several genes regulated by DNCB and counterregulated by QMR were identified through transcriptome analysis in mouse skin, and RNA silencing experiments on these genes in TNF-α/IFN-γ- or DNCB-treated human keratinocytes revealed that IL36G and SPRR2B play important roles in inflammation and keratinization. The expression of IL36G and SPRR2B was significantly reduced by QMR in skin of DNCB-induced AD mice. These results underscore the promising role of QMR in ameliorating AD characterized by inflammation and skin lesion hyperkeratosis via targeting IL36G and SPRR2B. [BMB Reports 2025; 58(5): 209-216].

Indexed as

Dermatitis, AtopicAnimalsDinitrochlorobenzeneDisease Models, AnimalFemaleHumansInflammationKeratinocytesMiceMice, Inbred BALB CSkinDinitrochlorobenzene

Identifiers

PMID39757204
PMCPMC12123202

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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.