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Molecules 2015, 20(11), 20297-20311; doi:10.3390/molecules201119693

Derinat Protects Skin against Ultraviolet-B (UVB)-Induced Cellular Damage

1
The Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, 1 University Road, Tainan 70101, Taiwan
2
Lipid Science and Aging Research Center, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
3
Graduate Institute of Medicine, School of Medicine, Kaohsiung Medical University, No. 100, Shih-Chuan 1st Road, Kaohsiung 80708, Taiwan
4
Laboratory of Pathophysiology, Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8581, Japan
5
Department of Dermatology, Kaohsiung Medical University, No. 100, Shih-Chuan 1st Road, Kaohsiung 80708, Taiwan
6
School of High-Technology for Human Welfare, Tokai University, 410-0321 Numazu, Shizuoka, Japan
7
National Health Research Institutes, Distinguished Investigator, National Environmental Health Research Center, No. 35, Keyan Road, Zhunan Town, Miaoli County 35053, Taiwan
8
School of Pharmacy, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
9
Center for Stem Cell Research, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
10
Department of Physiology, College of Medicine, National Cheng Kung University, 1 University Road, Tainan 70101, Taiwan
*
Authors to whom correspondence should be addressed.
Academic Editor: Maurizio Battino
Received: 12 August 2015 / Revised: 29 October 2015 / Accepted: 5 November 2015 / Published: 12 November 2015
(This article belongs to the Collection Bioactive Compounds)
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Abstract

Ultraviolet-B (UVB) is one of the most cytotoxic and mutagenic stresses that contribute to skin damage and aging through increasing intracellular Ca2+ and reactive oxygen species (ROS). Derinat (sodium deoxyribonucleate) has been utilized as an immunomodulator for the treatment of ROS-associated diseases in clinics. However, the molecular mechanism by which Derinat protects skin cells from UVB-induced damage is poorly understood. Here, we show that Derinat significantly attenuated UVB-induced intracellular ROS production and decreased DNA damage in primary skin cells. Furthermore, Derinat reduced intracellular ROS, cyclooxygenase-2 (COX-2) expression and DNA damage in the skin of the BALB/c-nu mice exposed to UVB for seven days in vivo. Importantly, Derinat blocked the transient receptor potential canonical (TRPC) channels (TRPCs), as demonstrated by calcium imaging. Together, our results indicate that Derinat acts as a TRPCs blocker to reduce intracellular ROS production and DNA damage upon UVB irradiation. This mechanism provides a potential new application of Derinat for the protection against UVB-induced skin damage and aging. View Full-Text
Keywords: Derinat; UVB; ROS; calcium; TRPCs Derinat; UVB; ROS; calcium; TRPCs
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Hsu, W.-L.; Lu, J.-H.; Noda, M.; Wu, C.-Y.; Liu, J.-D.; Sakakibara, M.; Tsai, M.-H.; Yu, H.-S.; Lin, M.-W.; Huang, Y.-B.; Yan, S.-J.; Yoshioka, T. Derinat Protects Skin against Ultraviolet-B (UVB)-Induced Cellular Damage. Molecules 2015, 20, 20297-20311.

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