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

BMB Rep

Department of Pharmacology, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea; Department of Medical Sciences, Graduate School, The Catholic University of Korea, Seoul 06591, Korea; Institute for Aging and Metabolic Diseases, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea.

Published: January 2025

AI Article Synopsis

  • Atopic dermatitis (AD) is a chronic skin condition that causes itching and inflammation, often treated with corticosteroids like dexamethasone for temporary relief, but not as a cure.
  • Researchers explored a new non-invasive treatment called quantum molecular resonance (QMR), which showed promise in reducing AD-like skin lesions in a mouse model, minimizing immune cell infiltration and epidermal thickening.
  • Transcriptome analysis identified genes, specifically IL36G and SPRR2B, that's linked to inflammation and skin changes; QMR significantly decreased their expression, suggesting QMR could be a potential new therapy for AD.

Article 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.

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

BMB Rep

January 2025

Department of Pharmacology, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea; Department of Medical Sciences, Graduate School, The Catholic University of Korea, Seoul 06591, Korea; Institute for Aging and Metabolic Diseases, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea.

Article Synopsis
  • Atopic dermatitis (AD) is a chronic skin condition that causes itching and inflammation, often treated with corticosteroids like dexamethasone for temporary relief, but not as a cure.
  • Researchers explored a new non-invasive treatment called quantum molecular resonance (QMR), which showed promise in reducing AD-like skin lesions in a mouse model, minimizing immune cell infiltration and epidermal thickening.
  • Transcriptome analysis identified genes, specifically IL36G and SPRR2B, that's linked to inflammation and skin changes; QMR significantly decreased their expression, suggesting QMR could be a potential new therapy for AD.
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Identifying the set of genes collectively responsible for causing a disease from differential gene expression data is called gene selection problem. Though many complex methodologies have been applied to solve gene selection, formulated as an optimization problem, this study introduces a new simple, efficient, and biologically plausible solution procedure where the collective power of the targeted gene set to discriminate between diseased and normal gene expression profiles was focused. It uses Simulated Annealing to solve the underlying optimization problem and termed here as Differential Gene Expression Based Simulated Annealing (DGESA).

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