Background and Purposes : Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by immune dysregulation and barrier dysfunction. Orientin, a flavonoid compound, has shown potential anti-inflammatory properties. This study investi...
Background and Purposes : Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by immune dysregulation and barrier dysfunction. Orientin, a flavonoid compound, has shown potential anti-inflammatory properties. This study investigates the effects of orientin on inflammatory responses in keratinocytes and its therapeutic potential in an AD-like animal model.
Materials and methods : HaCaT cells, a human keratinocyte line, were treated with varying concentrations of orientin to assess its effects on cell viability, cytokine production, and skin barrier function. RT-PCR and Western blot analyses were conducted to evaluate the expression of involucrin (INV) and filaggrin (FLG), as well as the activation of MAPK signaling pathways. In vivo, an AD-like mouse model was induced using dinitrochlorobenzene (DNCB), and the effects of orientin on AD symptoms, serum IgE levels, skin thickness, and T cell infiltration were examined.
Results and conclusions : Orientin treatment did not significantly affect INV expression but showed a trend towards increasing FLG expression at concentrations of 12.5 and 25 μM. In HaCaT cells, orientin significantly inhibited ERK phosphorylation without affecting JNK and p38 MAPK activation. In the AD-like animal model, orientin reduced AD symptoms, decreased serum IgE levels, and attenuated inflammatory cell infiltration in skin lesions. Orientin exhibits anti-inflammatory effects by modulating skin barrier function and MAPK signaling pathways in keratinocytes, and it alleviates symptoms in an AD-like animal model. These findings suggest that orientin may be a promising candidate for the treatment of AD.
Keywords : Orientin, Atopic dermatitis, Keratinocytes, Inflammation, Skin barrier function, MAPK signaling, Cytokine production, Filaggrin, ERK phosphorylation, Animal model.