發明
美國
13/445,451
US 8,772,347 B2
用於促進皮膚細胞增生及/或遷移的組成物、生薑萃取物及其醫藥組成物Use of a pharmaceutical composition for promoting proliferation and/or migration of skin cells, and for improving wound healing in a subject
高雄醫學大學
2014/07/08
我們由食用生薑中純化得一化合物6-dehydrogingerdione (6-DG),可促進人類皮膚細胞生長(表皮的角質層細胞與真皮的纖維母細胞)。增進效果濃度由高至低呈遞增的趨勢,最佳為2 M。在體外的創傷修復實驗中(12 or 24 h),6-DG加速了纖維母細胞與角質層細胞的爬行速度。同時也提高了三種生長因子的產量[transforming growth factor- (TGF-), platelet derived growth factor-αs (PDGF-αs) and vascular endothelial growth factors]。纖維母細胞所產生的膠原蛋白也隨著6-DG濃度上升而增加。在phorbol 12-myristate 13-acetate (PMA)的前處理下,6-DG降低了matrix metalloproteinase-1 (MMP-1)的蛋白質量及活性,恢復了phorbol 12-myristate 13-acetate (PMA)的產量。我們證明6-DG藉由降低c-Jun 和 p-ERK以抑制MAPK pathway,將可成為皮膚修復的藥物。 We identified one Zingiber officinale compound, 6-dehydrogingerdione (6-DG), promoted normal human skin cell growth. The treatments accelerate cell growth, the effectiveness of the concentrations decreased from high to low dose. In the in vitro wound healing assay for 12 or 24 h, 6-DG precipitated fibroblasts and keratinocytes migration. 6-DG-treated fibroblasts and keratinocytes showed higher growth factor productions in TGF-s, platelet derived growth factor-αs (PDGF-αs) and vascular endothelial growth factors (VEGF). Moreover, 6-DG increased fibroblasts collagen yield in a dose-dependent manner. 6-DG reduced matrix metalloproteinase-1 (MMP-1) protein level and activity, and recovered tissue inhibitor of metalloproteinase-1 (TIMP-1) under phorbol 12-myristate 13-acetate (PMA) incubation. 6-DG blocked the MAPK pathway by the suppression of c-Jun and p-ERK in fibroblasts. Thus, this work provided the molecular basis of 6-DG as a novel potential wound repair agent.
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