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Molecular Medicine Reports 2020-Jul

Solanum nigrum Linne improves DNCB‑induced atopic dermatitis‑like skin disease in BALB/c mice

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Sooyeon Hong
Bina Lee
Jae-Hyun Kim
Eun-Young Kim
Minsun Kim
Boguen Kwon
Hye-Rin Cho
Youngjoo Sohn
Hyuk-Sang Jung

Mots clés

Abstrait

The present study aimed to investigate the effects of Solanum nigrum Linne (SNL) in a model of 1‑chloro‑2,4‑dinitrobenzene (DNCB)‑induced atopic dermatitis (AD) and in TNF‑α/IFN‑γ‑stimulated HaCaT cells. AD is a chronic inflammatory skin disease and is characterized by erythema, edema, increased pruritus and eczema. Steroids are most commonly used for anti‑inflammatory therapy; however, their long‑term use is limited due to side‑effects, such as osteoporosis, brittle skin, muscle weaknesses and diabetes. Therefore, patients with AD require alternative treatment strategies. In previous studies, SNL has been reported to be effective against oxidants and cancer. However, to the best of our knowledge, the effects of SNL on AD have not yet been investigated. The present study examined the effects of SNL ethanol extract on a model of DNCB induced AD and on TNF‑α/IFN‑γ‑stimulated HaCaT cells. The skin tissue was sectioned to measure the thicknesses of the epidermis and dermis, as well as the numbers of eosinophils, mast cells and CD8 infiltration by H&E, toluidine blue, Masson's trichrome and IHC staining. ELISA was performed using serum to measure IgE levels. The present study also examined the expression of various inflammatory cytokines, MAPK and NF‑κB in TNF‑α/IFN‑γ‑stimulated HaCaT cells. SNL significantly reduced the levels of cytokines released from HaCaT cells stimulated with TNF‑α/IFN‑γ. SNL also significantly reduced the levels of p‑p38 at 30 min and significantly reduced the activation of NF‑κB in a time course experiment. In addition, SNL significantly reduced the level of serum IgE and dermal thickness and the infiltration of mast cells and CD8 in the BALB/c mouse model of DNCB‑induced AD. The results of the current study suggest that SNL exerts a suppressive effect on pro‑inflammatory cytokines in vitro and in vivo through the regulation of the immune system.

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