Rhododendrin inhibits toll-like receptor-7-mediated psoriasis-like skin inflammation in mice

Many active compounds present in Rhododendron brachycarpum have been used in traditional Oriental medicine for the treatment of various skin diseases. However, the precise mechanism of action of the compounds isolated from R. brachycarpum and their relevance as therapeutics for the treatment of psoriasis remain elusive. In this study, we report that rhododendrin isolated from R. brachycarpum strongly inhibits imiquimod (IMQ)-induced psoriasis-like skin inflammation in mice. We showed that topical treatment with rhododendrin reduces IMQ-induced skin hyperplasia, inflammatory mononuclear cell infiltration and the expression of pro-inflammatory mediators in mouse skin. In addition, we found that rhododendrin inhibits the activation of the TLR-7/NF-κB and mitogen-activated protein kinase pathways in both IMQ-induced psoriasis-like skin inflammation in mice and in normal human epidermal keratinocytes treated with IMQ. These results suggest that rhododendrin has an anti-inflammatory effect and can be used as a therapeutic to fight against psoriasis and other inflammatory skin diseases.

Effects of VitabridC¹² on Skin Inflammation

BACKGROUND: VitabridC¹² is newly developed and composed of vitamin C and Vitabrid (lamellar, hydrated zinc oxide). OBJECTIVE: In this study, we aimed to investigate the effects of VitabridC¹² on psoriasis and atopic dermatitis. METHODS: Mice with imiquimod-induced psoriasis or Dermatophagoides farinae-induced atopic dermatitis were applied with VitabridC¹². The effects of VitabridC¹² were evaluated by clinical features, histology, and immunologic features by examining cytokines and chemokines. RESULTS: In psoriasis model, VitabridC¹² decreased epidermal thickness and reduced inflammatory cell infiltration. In atopic dermatitis model, VitabridC¹² decreased dermal infiltration of inflammatory cells, epidermal hyperplasia, and hyperkeratosis. VitabridC¹² reduced the expression levels of proinflammatory mediators such as interleukin (IL)-1β, IL-6, IL-8, IL-17A, IL-22, tumor necrosis factor-α, CXCL1, CCL17, and CCL20 as well as COX-2 in imiquimod-induced psoriatic skin lesions. Likewise, VitabridC¹² reduced the expression levels of IL-4, IL-5, IL-13, thymic stromal lymphopoietin, and CCL4 in D. farinae-induced skin lesions, and decreased the serum immunoglobulin E level in the atopic dermatitis mouse model. Particularly, the VitabridC¹²-treated mice showed downregulated expressions of mitogen-activated protein kinase (MAPK), including extracellular signal-regulated kinase (ERK), p38, and MAPK/ERK kinase, as well as inhibited phosphorylation of nuclear factor-κB p65. CONCLUSION: Taken together, these findings indicate that VitabridC¹² exhibits anti-inflammatory activities and is a promising candidate as a treatment option for psoriasis or atopic dermatitis.