Abstract
Skin fibrotic diseases, such as keloids, are mainly caused by pathologic scarring of wounds during healing and characterized by benign cutaneous overgrowths of dermal fibroblasts. Current surgical and therapeutic modalities of skin fibrosis are unsatisfactory. Pinocembrin, a natural flavonoid, has been shown to possess a vast range of pharmacological activities including antimicrobial, antioxidant, anti-inflammatory, and anti-tumor activities. In this study we explored the potential effect and mechanisms of pinocembrin on skin fibrosis in vitro and in vivo. In vitro studies indicated that pinocembrin dose-dependently suppressed proliferation, migration, and invasion of keloid fibroblasts and mouse primary dermal fibroblasts. The in vivo studies showed that pinocembrin could effectively alleviate bleomycin (BLM)-induced skin fibrosis and reduce the gross weight and fibrosis-related protein expression of keloid tissues in xenograft mice. Further mechanism studies indicated that pinocembrin could suppress TGF-β1/Smad signaling and attenuate TGF-β1-induced activation of skin fibroblasts. In conclusion, our results demonstrate the therapeutic potential of pinocembrin for skin fibrosis.
Highlights
Skin fibrosis is a pathological result of abnormal tissue repair after deep skin dermis injury and occurs in a variety of pathological processes, such as immune disease scleroderma (SSc), keloids, and hypertrophic scars (HS) [1,2]
Results of MTT experiments showed that the IC50 value of pinocembrin in dermal fibroblasts (DFs) was between 336.9 μM and 380.6 μM (Figure S1)
Since excessive and abnormal proliferation of fibroblasts has been reported in keloids, we evaluated the regulatory function of pinocembrin on the proliferation of keloid fibroblasts (KFs) by using the Cell Counting Kit-8 (CCK-8) assay
Summary
Skin fibrosis is a pathological result of abnormal tissue repair after deep skin dermis injury and occurs in a variety of pathological processes, such as immune disease scleroderma (SSc), keloids, and hypertrophic scars (HS) [1,2]. Keloids are a skin fibrotic disease characterized by excessive deposition of extracellular matrix such as collagen in the dermis and subcutaneous tissues caused by human skin injuries, burns, or surgery [3]. Keloid scars relapse after simple surgical resection, and the side effects of therapeutic drugs are relatively numerous [5]. Recent studies have shown that excessive proliferation of fibroblasts, extracellular matrix deposition, and inflammatory cell infiltration in the process of tissue repair together constitute the biological basis of keloid formation [6].
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