論文

2019年11月1日

Protective Effects of 2',3'-Dihydroxy-4',6'-dimethoxychalcone Derived from Green Perilla Leaves against UV Radiation-Induced Cell Injury in Human Cultured Keratinocytes.

Biological & pharmaceutical bulletin
  • Yuki Takada-Takatori
  • ,
  • Yuri Tomii
  • ,
  • Shota Takemasa
  • ,
  • Yuka Takeda
  • ,
  • Yasuhiko Izumi
  • ,
  • Akinori Akaike
  • ,
  • Katsuharu Tsuchida
  • ,
  • Toshiaki Kume

42
11
開始ページ
1936
終了ページ
1941
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1248/bpb.b19-00618

Skin exposure to UV rays causes the production of reactive oxygen species (ROS), and it is a major risk factor for various skin disorders and diseases. In particular, exposure to UV-A is a major cause of photoaging. We have previously isolated 2',3'-dihydroxy-4',6'-dimethoxychalcone (DDC) from green perilla leaves as an activator of the nuclear factor erythroid 2-related factor-2 (Nrf2)-antioxidant response element (ARE) and demonstrated the protective effects of DDC both in vitro and in vivo in PC12 cells and Parkinson's disease models, respectively. In this study, we used HaCaT cells to examine the effects of DDC on ROS production and cell damage induced by UV-A. Our results indicated that UV-A irradiation in HaCaT cells increased ROS production in an energy-dependent manner. In addition, cell viability decreased in an energy-dependent manner 24 h after UV-A irradiation. However, treatment with DDC 24 h prior to UV-A irradiation significantly suppressed UV-A radiation-induced ROS production. In addition, DDC showed cytoprotective effects when used 24 h before and after UV-A irradiation. Treatment with DDC for 24 h also increased the expression levels of heme oxygenase-1 (HO-1) in a concentration-dependent manner. Pretreatment with the HO-1 inhibitor followed by DDC treatment before UV-A irradiation for 24 h reduced ROS production and the cytoprotective effect. These results suggest that DDC increases the expression levels of HO-1 and protects HaCaT cells through the suppression of UV radiation-induced ROS production.

リンク情報
DOI
https://doi.org/10.1248/bpb.b19-00618
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/31462615
ID情報
  • DOI : 10.1248/bpb.b19-00618
  • PubMed ID : 31462615

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