Details

Autor(en) / Beteiligte

• Liu, Xiao‐yi
• Hwang, Eunson
• Park, Bom
• Ngo, Hien T. T.
• Xiao, Yong‐kun
• Yi, Tae‐Hoo

Titel

Ginsenoside C‐Mx Isolated from Notoginseng Stem‐leaf Ginsenosides Attenuates Ultraviolet B‐mediated Photoaging in Human Dermal Fibroblasts

Ist Teil von

• Photochemistry and photobiology, 2018-09, Vol.94 (5), p.1040-1048

Ort / Verlag

United States: Blackwell Publishing Ltd

Erscheinungsjahr

2018

Quelle

Wiley Online Library All Journals

Beschreibungen/Notizen

• Notoginseng is a traditional herbal medicine widely used for medicinal therapy in Asia, as it contains numerous ginsenosides with pharmacological effects. In this study, we submitted Notoginseng stem‐leaf (NGL) ginsenosides to an enzyme to create a reaction with the monomer products of ginsenoside C‐Mx and then investigated the ability of ginsenoside C‐Mx to protect the skin against ultraviolet B‐induced injury in normal human dermal fibroblasts (NHDFs). Ginsenoside C‐Mx alleviated UVB‐induced intracellular reactive oxygen species (ROS), MMP‐1 and IL‐6 expression while accelerating TGF‐β and procollagen type I secretion. In addition, ginsenoside C‐Mx reversed UVB‐induced procollagen type I reduction by regulating the TGF‐β/Smad signaling pathway. Moreover, ginsenoside C‐Mx inhibited activation of AP‐1 transcription factor, an inducer of MMPs. Ginsenoside C‐Mx displayed an outstanding antioxidant capacity, increasing expression of cytoprotective antioxidants such as HO‐1 and NQO‐1 expression by enhancing the nuclear accumulation of Nrf2. Interestingly, application of ginsenoside C‐Mx treatment (1, 10, 20 μm) significantly diminished UVB‐induced suppressed NF‐κB expression, decreasing the over‐released inflammatory cytokines. Taken together, our findings indicated that ginsenoside C‐Mx may act as a promising natural cosmetic ingredient for prevention and treatment of UVB‐induced skin damage. Chronic exposure to UV radiation results in skinphotoaging, clinically accompanied with loss of elasticity and tension. In this study, we demonstrated that ginsenoside C‐Mx could reverse this damage via increasing procollagen synthesis and blocking MMPs, inflammatory factors expression. The studies of molecular mechanism indicated ginsenoside C‐Mx could inhibit MMPs expression via inactivating MAPK/AP‐1, NF‐κB pathway and accelerate type I procollagen synthesis through activating the TGF‐β/Smad pathway. Furthermore, ginsenoside C‐Mx reduced UVB‐enhanced ROS via promoting Nrf2 nuclear location and enhancing the expression of cytoprotective antioxidants.