Atopic dermatitis (AD) is a chronic and allergic skin disease; however, there is no cure for the disease. Red ginseng is well known to have anti-AD potential, while red ginseng marc (RGM) remaining after ginseng extraction is regarded as useless and discarded. However, it has recently been reported that RGM, particularly fermented RGM (fRGM), still contains bioactive properties. Thus, the anti-allergic effects of fRGM were examined in a 2,4-dinitrochlorobenzene-induced AD-like mice model. The model was topically treated with distilled water (control), dexamethasone, or fRGM for six weeks. Treatments of fRGM alleviated skin lesions and reduced serum IgE levels, compared with the control. The fRGM also reduced skin levels of lipid peroxidation and superoxide anion; however, it increased glutathione contents, with downregulated gene expression for inflammatory mediators. Histopathological analyses demonstrated that fRGM suppressed epidermal thickening, collagen deposition, and inflammatory cell and mast cell infiltration, which involved anti-inflammatory, antioxidant, and anti-apoptotic effects. Further, fRGM suppressed hypertrophic changes and inflammatory responses in the spleen and lymph nodes. The beneficial effects were observed in the dexamethasone and fRGM groups; however, the antioxidant effects were evident only in the fRGM treatments. These results provide useful information for developing fRGM as a therapeutic source for AD.

Atopic dermatitis (AD) is a chronic and allergic skin disease, however, there is no cure for the disease. Many studies have shown anti-AD potentials of red ginseng, while red ginseng marc (RGM) remained after the ginseng extraction is discarded as industrial waste. However, it is recently reported that RGM, particularly fermented RGM (fRGM), still contains the bioactive properties. Thus, anti-allergic effects of fRGM were examined in 2,4-dinitrochlorobenzene-induced AD-like mice model. The model was topically treated with distilled water (control), dexamethasone, or fRGM for six weeks. The treatments of fRGM alleviated the skin lesions and reduced serum IgE levels, compared with the control. The fRGM also reduced skin levels of lipid peroxidation and superoxide anion, however, increased glutathione contents, with down-regulated gene expressions for inflammatory mediators. The histopathological analyses demonstrated that fRGM suppressed the epidermal thickening, collagen deposition, and inflammatory cell and mast cell infiltration, which involved the anti-inflammatory, anti-oxidant, and anti-apoptotic effects. Further, fRGM suppressed hypertrophic changes and inflammatory responses in the spleen and lymph node. The beneficial effects were observed in the dexamethasone and fRGM groups, however, the antioxidant effects were evident only in the fRGM treatments. These provide useful information for developing fRGM as therapeutic sources for AD.