Atopic dermatitis (AD) is a chronic inflammatory skin disease that seriously affects quality of life. Quinine is a bitter taste receptor agonist that exhibits antimalarial effects. The aim of the present study was to examine the therapeutic effects of quinine in AD‑like mice. AD was induced with 2,4‑dinitrochlorobenzene, and the mice were treated with 10 mg/kg quinine for 1, 4 and 7 days. A total of 60 BALB/c mice were divided into the following groups: Healthy, AD‑like, AD‑like + quinine and healthy + quinine, with 1, 4 and 7 days groups for each treatment. Blood was extracted from all mice and ELISA was performed to detect immunoglobulin E (IgE) levels. H&E‑stained tissue sections were prepared from skin lesions on the backs of the mice and pathological changes were observed. Cytokines were detected via ELISA, and the filaggrin (FLG) and kallikrein‑7 (KLK7) proteins were detected via western blotting and immunohistochemistry. IKKα and NF‑κB mRNA were analyzed via reverse transcription‑quantitative PCR. Quinine ameliorated skin damage in the AD‑like mice, reduced IgE expression in the blood, inhibited expression of IKKα and NF‑κB, reduced cytokine secretion, reduced KLK7 expression, reduced scratching frequency, increased FLG expression and repaired the skin barrier. These results suggested that quinine exhibited therapeutic effects in AD‑like mice.
Keywords: NF‑κB signaling pathway; atopic dermatitis; quinine.