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Peer-reviewed veterinary case report

A preclinical study of device dependent therapeutic effects of cold atmospheric plasmas on atopic dermatitis induced by DNCB.

Journal:
Scientific reports
Year:
2026
Authors:
Shakeri, Fatemeh et al.
Affiliation:
Plasma Research Institute
Species:
rodent

Abstract

Atopic dermatitis (AD) is a skin disease resulting from a complex interplay between genetic factors, environmental influences, microbiota, skin barrier dysfunction, and immune system disorders. Despite the existence of various AD therapies, it is necessary to develop new therapies for AD treatment. Cold atmospheric plasma (CAP) is a promising non-invasive therapeutic alternative in dermatology. This study aims to investigate the device-dependent effects of CAP sources in treating a 1-chloro-2,4-dinitrobenzene(DNCB)-induced AD model in Balb/c mice, comparing its effects with an immunosuppressive drug. AD-like skin disease was induced by DNCB in female BALB/c mice. Mice were treated with cold plasma and tacrolimus ointment (TAC). Skin inflammation was assessed by histopathological analysis. IHC staining was performed for CD31 and E-cadherin to investigate of level of angiogenesis and expression of adherens junction protein. Cytokine expression was determined by quantitative real-time PCR. Our results demonstrate that helium and argon plasma were more effective than air plasma and TAC in reducing clinical symptoms and histopathological damage (particularly epidermis and dermis). CAP treatments showed a more pronounced decrease in the levels of inflammatory cytokines IL-13, IL-31, and IL-12 compared to the AD group (p&#x2009;<&#x2009;0.01). Argon and air plasma treatment significantly reduced mast cell infiltration more than helium plasma treatment. Additionally, helium and argon plasma treatment enhanced cell adhesion protein E-cadherin and modulated CD31 protein, a marker of angiogenesis. Together, these findings suggest that CAP may be a promising candidate for the research and development of therapeutic modalities for AD.

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Original publication: https://pubmed.ncbi.nlm.nih.gov/41617812/