Details

Autor(en) / Beteiligte

• Gao, Wei
• Wang, Yu‐shuai
• Qu, Zheng‐yi
• Hwang, Eunson
• Ngo, Hien T. T.
• Wang, Ying‐ping
• Bae, Jahyun
• Yi, Tae‐hoo

Titel

Orobanche cernua Loefling Attenuates Ultraviolet B‐mediated Photoaging in Human Dermal Fibroblasts

Ist Teil von

• Photochemistry and photobiology, 2018-07, Vol.94 (4), p.733-743

Ort / Verlag

United States: Blackwell Publishing Ltd

Erscheinungsjahr

2018

Quelle

Wiley-Blackwell Journals

Beschreibungen/Notizen

• UV radiation is the primary cause of skin photoaging, which results in an increase in matrix metalloproteinases and degradation of collagen. Developing new natural antioxidant as photoprotective agents has become a popular area of research. Orobanche cernua Loefling is a parasitic plant that is rich in phenylethanoid glycosides (PhGs). This study investigated the photoprotective effects of the ethanolic extract of Orobanche cernua Loefling (OC) and its principal component acteoside on UVB‐induced photoaging as well as their underlying molecular mechanisms in normal human dermal fibroblasts (NHDFs). Biological testing demonstrated that OC and acteoside possessed significant photoprotective activities, reducing MMP and IL‐6 levels while improving type‐I procollagen synthesis in UVB‐irradiated NHDFs. Further study showed that the protective mechanisms were the improvement of transcription factor Nrf2‐mediated antioxidant defensive system, suppression of MAPK/AP‐1 and activation of the TGF‐β/Smad pathway. Together, our results suggested that OC might be a promising antiphotoaging agent against UV radiation‐induced skin damage. Chronic exposure to UV radiation results in skin premature aging (photoaging), clinically accompanied with loss of elasticity and tension. In this study, we demonstrated that OC could reverse this damage via increasing procollagen synthesis and blocking MMPs expression. The studies of molecular mechanism indicated OC could inhibit MMPs expression via inactivating MAPK/AP‐1 pathway and accelerate type‐I procollagen synthesis through activating the TGF‐β/Smad pathway. Furthermore, OC reduced UVB‐enhanced ROS via promoting Nrf2 nuclear location and enhancing the expression of cytoprotective antioxidants.