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http://dx.doi.org/10.4062/biomolther.2015.005

Isorhamnetin Protects Human Keratinocytes against Ultraviolet B-Induced Cell Damage  

Han, Xia (School of Medicine, Jeju National University)
Piao, Mei Jing (School of Medicine, Jeju National University)
Kim, Ki Cheon (School of Medicine, Jeju National University)
Hewage, Susara Ruwan Kumara Madduma (School of Medicine, Jeju National University)
Yoo, Eun Sook (School of Medicine, Jeju National University)
Koh, Young Sang (School of Medicine, Jeju National University)
Kang, Hee Kyoung (School of Medicine, Jeju National University)
Shin, Jennifer H (Department of Mechanical Engineering & Graduate School of Medical Science and Engineering, KAIST)
Park, Yeunsoo (National Fusion Research Institute, Plasma Technology Research Center)
Yoo, Suk Jae (National Fusion Research Institute, Plasma Technology Research Center)
Chae, Sungwook (Aging Research Center, Korea Institute of Oriental Medicine)
Hyun, Jin Won (School of Medicine, Jeju National University)
Publication Information
Biomolecules & Therapeutics / v.23, no.4, 2015 , pp. 357-366 More about this Journal
Abstract
Isorhamnetin (3-methylquercetin) is a flavonoid derived from the fruits of certain medicinal plants. This study investigated the photoprotective properties of isorhamnetin against cell damage and apoptosis resulting from excessive ultraviolet (UV) B exposure in human HaCaT keratinocytes. Isorhamnetin eliminated UVB-induced intracellular reactive oxygen species (ROS) and attenuated the oxidative modification of DNA, lipids, and proteins in response to UVB radiation. Moreover, isorhamnetin repressed UVB-facilitated programmed cell death in the keratinocytes, as evidenced by a reduction in apoptotic body formation, and nuclear fragmentation. Additionally, isorhamnetin suppressed the ability of UVB light to trigger mitochondrial dysfunction. Taken together, these results indicate that isorhamnetin has the potential to protect human keratinocytes against UVB-induced cell damage and death.
Keywords
Isorhamnetin; Ultraviolet B; Reactive oxygen species; Human keratinocyte; Programmed cell death;
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