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Article

Ginsenoside Rc protects against UVB‑induced photooxidative damage in epidermal keratinocytes

  • Authors:
    • Yuri Oh
    • Hye‑Won Lim
    • Kwang Hark Park
    • Yu‑Hua Huang
    • Ji‑Young Yoon
    • Kyunghoon Kim
    • Chang‑Jin Lim
  • View Affiliations / Copyright

    Affiliations: Department of Biological Sciences, College of Natural Sciences, Kangwon National University, Chuncheon, Gangwon 24341, Republic of Korea, Shebah Biotech Inc., G‑Tech Village, Chuncheon, Gangwon 24398, Republic of Korea, Jeonju AgroBio‑Materials Institute, Jeonju, Jeollabuk 54810, Republic of Korea
  • Pages: 2907-2914
    |
    Published online on: July 6, 2017
       https://doi.org/10.3892/mmr.2017.6943
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Abstract

Ginsenoside Rc (Rc) is a major ginsenoside isolated from Panax ginseng, and has exhibited pharmacological effects on skin cells. The present study aimed to investigate the putative skin‑protective properties of Rc, including its anti‑photoaging and barrier function‑protective effects, in human HaCaT keratinocytes exposed to UVB radiation. The protective properties of Rc were evaluated through the assessment of keratinocyte viability, reactive oxygen species (ROS) production, total glutathione (GSH) and superoxide dismutase (SOD) activity, caspase‑14, matrix metalloproteinase (MMP)‑2 and ‑9 activity, and MMP‑2, MMP‑9 and filament aggregating protein (filaggrin) expression following UVB irradiation. Treatment with Rc was revealed to prevent the UVB‑induced increase in ROS production and pro‑MMP‑2 and ‑9 levels in HaCaT keratinocytes. In addition, treatment with Rc resulted in enriched GSH contents and enhanced SOD activity following exposure to UVB radiation. Furthermore, Rc treatment enhanced caspase‑14 activity and counteracted the UVB‑induced downregulation in filaggrin expression. However, no significant difference was identified between Rc‑treated and normal groups in terms of keratinocyte viability, regardless of exposure to radiation. The present findings suggested that Rc may exert anti‑photoaging and barrier function‑protective effects in keratinocytes, and thus protect the skin against photooxidative stress induced by exposure to UV radiation.
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Copy and paste a formatted citation
Spandidos Publications style
Oh Y, Lim HW, Park K, Huang YH, Yoon JY, Kim K and Lim CJ: Ginsenoside Rc protects against UVB‑induced photooxidative damage in epidermal keratinocytes. Mol Med Rep 16: 2907-2914, 2017.
APA
Oh, Y., Lim, H., Park, K., Huang, Y., Yoon, J., Kim, K., & Lim, C. (2017). Ginsenoside Rc protects against UVB‑induced photooxidative damage in epidermal keratinocytes. Molecular Medicine Reports, 16, 2907-2914. https://doi.org/10.3892/mmr.2017.6943
MLA
Oh, Y., Lim, H., Park, K., Huang, Y., Yoon, J., Kim, K., Lim, C."Ginsenoside Rc protects against UVB‑induced photooxidative damage in epidermal keratinocytes". Molecular Medicine Reports 16.3 (2017): 2907-2914.
Chicago
Oh, Y., Lim, H., Park, K., Huang, Y., Yoon, J., Kim, K., Lim, C."Ginsenoside Rc protects against UVB‑induced photooxidative damage in epidermal keratinocytes". Molecular Medicine Reports 16, no. 3 (2017): 2907-2914. https://doi.org/10.3892/mmr.2017.6943
Copy and paste a formatted citation
x
Spandidos Publications style
Oh Y, Lim HW, Park K, Huang YH, Yoon JY, Kim K and Lim CJ: Ginsenoside Rc protects against UVB‑induced photooxidative damage in epidermal keratinocytes. Mol Med Rep 16: 2907-2914, 2017.
APA
Oh, Y., Lim, H., Park, K., Huang, Y., Yoon, J., Kim, K., & Lim, C. (2017). Ginsenoside Rc protects against UVB‑induced photooxidative damage in epidermal keratinocytes. Molecular Medicine Reports, 16, 2907-2914. https://doi.org/10.3892/mmr.2017.6943
MLA
Oh, Y., Lim, H., Park, K., Huang, Y., Yoon, J., Kim, K., Lim, C."Ginsenoside Rc protects against UVB‑induced photooxidative damage in epidermal keratinocytes". Molecular Medicine Reports 16.3 (2017): 2907-2914.
Chicago
Oh, Y., Lim, H., Park, K., Huang, Y., Yoon, J., Kim, K., Lim, C."Ginsenoside Rc protects against UVB‑induced photooxidative damage in epidermal keratinocytes". Molecular Medicine Reports 16, no. 3 (2017): 2907-2914. https://doi.org/10.3892/mmr.2017.6943
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