ArticleMolecular and cellular biochemistry2026
Wogonin alleviates inflammation caused by neutrophil extracellular traps in atopic dermatitis via miR-4667-5p/CCL2 pathway.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Atopic dermatitis (AD) is primarily characterized by dysregulation of the immune system and abnormal inflammation. Dictamni Cortex is an herb used in traditional Chinese medicine to treat damp-heat skin diseases. To excavate the effective component of Dictamni Cortex for treating AD and explore the specific molecular mechanism. First, wogonin was screened from the active constituents of Dictamnus cortex, and CCL2 was identified as a candidate hub gene by constructing an herb-ingredient-gene network. The AD cell model was constructed using human epidermal keratinocytes (HEKs), and the AD mouse model was employed to investigate the therapeutic efficacy of wogonin. The effect of HEKs on neutrophil extracellular trap (NET) formation under pathological conditions was explored through co-culture experiments. The conditional medium containing NETs was used to treat HEKs to investigate AD-associated inflammatory alterations. Through bioinformatics means, miR-4667-5p was predicted as an upstream regulator targeting CCL2 mRNA, and this was validated via RNA pull-down and dual-luciferase reporter assays. CCL2 was significantly upregulated in the AD cell model, which mediated the functional damage of HEKs under AD pathological conditions. Wogonin not only rescued the cell viability of HEKs in a concentration-dependent manner by inhibiting CCL2 but also alleviated the AD-related inflammation in vitro and in vivo. Within the co-culture system, AD model cells recruited neutrophils and induced NET formation, which was suppressed following CCL2 knockdown. Overexpression of miR-4667-5p suppressed CCL2 expression by targeting its mRNA and alleviated inflammation in HEKs induced by NET-conditioned medium. This inflammation was also suppressed by wogonin treatment. The miR-4667-5p antagonist weakened this therapeutic effect of wogonin, which was rescued by the silencing of CCL2. Under AD pathological conditions, HEKs promoted NET formation, which in turn exacerbated inflammation within HEKs. Wogonin treatment rescued this inflammatory damage by modulating the miR-4667-5p/CCL2 pathway.
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