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

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 2ʹ,3ʹ-dihydroxy-4ʹ,6ʹ-dimethoxychalcone (DDC) from green...

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Bibliographic Details
Published in:Biological & pharmaceutical bulletin 2019/11/01, Vol.42(11), pp.1936-1941
Main Authors: Takada-Takatori, Yuki, Tomii, Yuri, Takemasa, Shota, Takeda, Yuka, Izumi, Yasuhiko, Akaike, Akinori, Tsuchida, Katsuharu, Kume, Toshiaki
Format: Article
Language:eng ; jpn
Subjects:
Animals
antioxidant enzyme
Cell Line
Cell Survival - drug effects
Chalcones - pharmacology
HaCaT cell
Heme Oxygenase-1 - metabolism
Humans
inflammation
Keratinocytes
NF-E2-Related Factor 2
nuclear factor-erythroid 2-related factor-2–antioxidant response element pathway
oxidative stress
Perilla
Plant Extracts - pharmacology
Reactive Oxygen Species - metabolism
Skin - metabolism
Ultraviolet Rays - adverse effects
UV-A irradiation
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Summary: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 2ʹ,3ʹ-dihydroxy-4ʹ,6ʹ-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.
ISSN:0918-6158
1347-5215
DOI:10.1248/bpb.b19-00618