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Journal of Environmental Pathology, Toxicology and Oncology
インパクトファクター: 1.625 5年インパクトファクター: 1.63 SJR: 0.402 SNIP: 0.613 CiteScore™: 2.3

ISSN 印刷: 0731-8898
ISSN オンライン: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.2016014003
pages 11-28

Photoprotective Effect of Carpomitra costata Extract against Ultraviolet B-Induced Oxidative Damage in Human Keratinocytes

J. Zheng
School of Medicine, Jeju National University, Jeju, Republic of Korea
S.R.K. Madduma Hewage
School of Medicine, Jeju National University, Jeju, Republic of Korea
Mei Jing Piao
School of Medicine, Jeju National University, Jeju, Republic of Korea
Kyoung Ah Kang
School of Medicine, Jeju National University, Jeju, Republic of Korea
X Han
School of Medicine, Jeju National University, Jeju, Republic of Korea
H.K. Kang
School of Medicine, Jeju National University, Jeju, Republic of Korea
E.S. Yoo
School of Medicine, Jeju National University, Jeju, Republic of Korea
Y.S. Koh
School of Medicine, Jeju National University, Jeju, Republic of Korea
N.H. Lee
Department of Chemistry, College of Natural Sciences, Jeju National University, Jeju, Republic of Korea
C. S. Ko
Jeju Biodiversity Research Institute, Jeju Technopark, Jeju, Republic of Korea
J. C. Lee
Jeju Biodiversity Research Institute, Jeju Technopark, Jeju, Republic of Korea
Mi Hee Ko
Jeju Biodiversity Research Institute, Jeju Technopark, Jeju, Republic of Korea
Jin Won Hyuna
School of Medicine, Jeju National University, Jeju, Republic of Korea

要約

Natural marine products show various biological properties such as antiphotoaging, antioxidant, anticancer, and anti-inflammation. This study evaluated the protective effects of the brown alga Carpomitra costata (Stackhouse) Batters (Sporochnaceae) against ultraviolet B (UVB)-provoked damage in human HaCaT keratinocytes. C. costata extract (CCE) effectively reduced superoxide anion, hydroxyl radical, and UVB-stimulated intracellular reactive oxygen species (ROS) levels. CCE also restored the expression and activity of UVB-suppressed antioxidant enzymes. Furthermore, CCE decreased UVB-triggered oxidative damage to cellular components including DNA, protein, and lipid and defended the cells against mitochondrial membrane depolarization-medicated apoptosis. The results of this study indicate that CCE can safeguard human keratinocytes against UVB-induced cellular damage via a potent antioxidant mechanism. CCE may find utility as part of a therapeutic arsenal against the damaging effects of UVB radiation on the skin.


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