ArticleMolecular medicine reports2016
Solanum tuberosum L. cv Hongyoung extract inhibits 2,4‑dinitrochlorobenzene‑induced atopic dermatitis in NC/Nga mice.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 12 citations in OpenAlex.
- Oral Administration ofAnimals : an open access journal from MDPI · 2026Article
- Phenolic and anthocyanin content characterization related to genetic diversity analysis ofFrontiers in plant science · 2022Article
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2 authors at 1 institution in 1 country.
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Abstract
Solanum tuberosum L. cv Hongyoung (SH) is a widely consumed anthocyanin-rich food and medicinal plant, which possesses anti‑inflammatory and anti‑allergic activities. The present study aimed to examine the inhibitory effects of SH extract on atopic dermatitis (AD)‑like skin lesions induced by the topical application of 2,4‑dinitrochlorobenzene (DNCB) in NC/Nga mice. SH extract was orally administered to the DNCB‑treated NC/Nga mice. The anti‑AD effects of SH extract were examined by measuring symptom severity; ear thickness; scratching behavior; serum levels of immunoglobulin (Ig)E; T‑helper (Th)1, Th2 and Th17 cytokine levels in the spleen; mRNA expression levels of inflammatory cytokines and chemokines; and tissue infiltration of inflammatory cells. The results demonstrated that SH extract inhibited the development of AD‑like lesions, and reduced IgE levels and the production of cytokines. Furthermore, SH extract significantly suppressed the expression of AD‑associated mRNAs in lesional skin. Histological alterations in the AD‑like lesions were visualized using hematoxylin and eosin, and toluidine blue staining in the DNCB‑treated group; the alterations were attenuated following SH treatment. In addition, thickening of the epidermis and accumulation of inflammatory cells in the DNCB‑treated mice were suppressed by SH treatment. These results suggested that SH extract may suppress the development of AD symptoms through modulation of the Th1 and Th2 responses.
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