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To investigate the effects of a digital electric fire-needling acupuncture device (EFNA) in a mouse model of chronic eczema (CE) and aimed to elucidate its underlying antipruritic mechanisms.
Forty bagg albino (BALB)/c mice were randomly assigned to 4 groups: control, model, EFNA, and halometasone groups (n = 10). Except for the control group, CE was induced in all groups using 2,4-dinitrochlorobenzene. After model establishment, mice in the EFNA group received EFNA treatment at the lesional skin sites, whereas the halometasone group received a dose-tapering regimen of topical halometasone for two weeks. The eczema area severity index of the dorsal skin, and scratching frequency (bouts/10 min) were assessed after model induction and treatment. The splenic index was recorded post-intervention. Hematoxylin and eosin staining evaluated skin morphology, and Western blot analysis determined expression levels of CXC motif chemokine ligand 10 (CXCL10), CXC chemokine receptor type 3 (CXCR3), mas-related g-protein coupled receptor member A3 (MrgprA3), and transient receptor potential vanilloid 1 (TRPV1) in skin tissue.
Both EFNA and halometasone markedly reduced eczema area severity index scores (both P < .001), significantly decreased scratching frequency (P = .010, P = .007), and reduced the spleen index (P = .029, P < .001). EFNA also alleviated edema and epidermal thickening in lesional skin, decreased local lymphocyte infiltration, and downregulated CXCL10, CXCR3, MrgprA3, and TRPV1 expression in skin tissues (all P < .001).
EFNA ameliorated 2,4-dinitrochlorobenzene-induced chronic eczematous lesions, with reductions in pruritus, inflammatory edema and cellular infiltration, alongside downregulation of CXCL10, CXCR3, MrgprA3, and TRPV1. These findings suggest that the antipruritic effect of EFNA may involve modulation of the non-histaminergic itch transmission pathway, providing new insights into the mechanism of fire-needling therapy for CE.
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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