Derinat protects skin against ultraviolet-B (UVB)-induced cellular damage

Wen Li Hsu, Jian He Lu, Mami Noda, Ching Ying Wu, Jia Dai Liu, Manabu Sakakibara, Ming Hsien Tsai, Hsin Su Yu, Ming Wei Lin, Yaw Bin Huang, Shian Jang Yan, Tohru Yoshioka

Research output: Contribution to journalArticle

9 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)20297-20311
Number of pages15
JournalMolecules
Volume20
Issue number11
DOIs
Publication statusPublished - 2015 Nov 12

Fingerprint

Skin
Sodium
sodium
damage
Reactive Oxygen Species
DNA Damage
oxygen
Skin Aging
deoxyribonucleic acid
DNA
Aging of materials
Transient Receptor Potential Channels
Immunologic Factors
Cyclooxygenase 2
cells
mice
calcium
Irradiation
Calcium
Imaging techniques

All Science Journal Classification (ASJC) codes

  • Analytical Chemistry
  • Chemistry (miscellaneous)
  • Molecular Medicine
  • Pharmaceutical Science
  • Drug Discovery
  • Physical and Theoretical Chemistry
  • Organic Chemistry

Cite this

Hsu, W. L., Lu, J. H., Noda, M., Wu, C. Y., Liu, J. D., Sakakibara, M., ... Yoshioka, T. (2015). Derinat protects skin against ultraviolet-B (UVB)-induced cellular damage. Molecules, 20(11), 20297-20311. https://doi.org/10.3390/molecules201119693
Hsu, Wen Li ; Lu, Jian He ; Noda, Mami ; Wu, Ching Ying ; Liu, Jia Dai ; Sakakibara, Manabu ; Tsai, Ming Hsien ; Yu, Hsin Su ; Lin, Ming Wei ; Huang, Yaw Bin ; Yan, Shian Jang ; Yoshioka, Tohru. / Derinat protects skin against ultraviolet-B (UVB)-induced cellular damage. In: Molecules. 2015 ; Vol. 20, No. 11. pp. 20297-20311.
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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.",
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Hsu, WL, Lu, JH, Noda, M, Wu, CY, Liu, JD, Sakakibara, M, Tsai, MH, Yu, HS, Lin, MW, Huang, YB, Yan, SJ & Yoshioka, T 2015, 'Derinat protects skin against ultraviolet-B (UVB)-induced cellular damage', Molecules, vol. 20, no. 11, pp. 20297-20311. https://doi.org/10.3390/molecules201119693

Derinat protects skin against ultraviolet-B (UVB)-induced cellular damage. / Hsu, Wen Li; Lu, Jian He; Noda, Mami; Wu, Ching Ying; Liu, Jia Dai; Sakakibara, Manabu; Tsai, Ming Hsien; Yu, Hsin Su; Lin, Ming Wei; Huang, Yaw Bin; Yan, Shian Jang; Yoshioka, Tohru.

In: Molecules, Vol. 20, No. 11, 12.11.2015, p. 20297-20311.

Research output: Contribution to journalArticle

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T1 - Derinat protects skin against ultraviolet-B (UVB)-induced cellular damage

AU - Hsu, Wen Li

AU - Lu, Jian He

AU - Noda, Mami

AU - Wu, Ching Ying

AU - Liu, Jia Dai

AU - Sakakibara, Manabu

AU - Tsai, Ming Hsien

AU - Yu, Hsin Su

AU - Lin, Ming Wei

AU - Huang, Yaw Bin

AU - Yan, Shian Jang

AU - Yoshioka, Tohru

PY - 2015/11/12

Y1 - 2015/11/12

N2 - 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.

AB - 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.

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Hsu WL, Lu JH, Noda M, Wu CY, Liu JD, Sakakibara M et al. Derinat protects skin against ultraviolet-B (UVB)-induced cellular damage. Molecules. 2015 Nov 12;20(11):20297-20311. https://doi.org/10.3390/molecules201119693