Rhododendron album Blume extract inhibits TNF-/IFN--induced chemokine production via blockade of NF-B and JAK/STAT activation in human epidermal keratinocytes

Rhododendron album Blume (RA) has traditionally been used as an herbal medicine and is considered to have anti-inflammatory properties. It is a well-known medicine for treatment of allergic or atopic diseases. In the present study, the biological effects of an RA methanol extract (RAME) on inflammation were investigated in tumor necrosis factor- (TNF-)/interferon- (IFN-)-stimulated human keratinocytes. The present study aimed to investigate the potential mechanisms by which RAME inhibited TNF-/IFN--induced expression of chemokines [thymus- and activation-regulated chemokine (TARC) and macrophage-derived chemokine (MDC)] and cytokines [interleukin (IL)-6 and IL-8] through the nuclear factor-B (NF-B) pathway in human keratinocytes. The effects of RAME treatment on cell viability were investigated in TNF-/IFN--stimulated HaCaT cells. The expression of TARC, MDC, IL-6 and IL-8 was assessed using reverse transcription-quantitative polymerase chain reaction analysis or ELISA, and its effect on the inhibitory mitogen-activated protein kinase pathway was also studied using western blot analysis. TNF-/IFN- induced the expression of IL-6, IL-8, TARC and MDC in a dose-dependent manner through NF-B and Janus kinase/signal transducers and activators of transcription (JAK/STAT) activation. Notably, treatment with RAME significantly suppressed TNF-/IFN--induced expression of IL-6, IL-8, TARC, and MDC. In addition, RAME treatment inhibited the activation of NF-B and the JAK/STAT pathway in TNF-/IFN--induced HaCaT cells. These results suggest that RAME decreases the production of chemokines and pro-inflammatory cytokines by suppressing the NF-B and the JAK/STAT pathways. Consequently, RAME may potentially be used for treatment of atopic dermatitis.