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KMID : 1150620180020010017
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Biomedical Dermatology
2018 Volume.2 No. 1 p.17 ~ p.17
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Antiapoptotic effects of scutellarin on ultraviolet A-irradiated HaCaT human keratinocytes
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Choi Mi-Na
Jeon See-Un
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Abstract
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Background: This study examines the cellular protective effects of scutellarin on HaCaT cells in which oxidative stress was induced by ultraviolet A (UVA).
Methods: Cell viability and lipid peroxidation were measured using WST-1 and MDA assays, respectively. The changes in cell number in the sub-G1 phase were assessed using cell cycle analysis, and tailed DNA levels were measured using the comet assay to examine the degree of DNA damage. The difference in the mitochondrial membrane potential was examined using JC-1 staining, and the regulation of BAX mRNA expression levels was examined using quantitative real-time polymerase chain reaction.
Results: Although UVA-irradiated cells resulted in a 3.63-fold increase in lipid peroxide, scutellarin-treated cells showed concentration-dependent decreases of 2.06, 1.39, and 0.97 times at scutellarin concentrations of 1, 5, and 10 μM, respectively. The cell number in the sub-G1 phase increased by 227% when irradiated by UVA but decreased to 187, 139, and 120% when cells were treated with scutellarin at concentrations of 1, 5, and 10 μM, respectively. Tailed DNA also showed a protective effect. The mitochondrial membrane potential difference decreased up to 36% when irradiated by UVA but recovered up to 58, 82, and 92% when cells were treated with scutellarin at concentrations of 1, 5, and 10 μM, respectively. BAX gene expression levels increased 9.7-fold by UVA but was downregulated to 7.4-, 4.71-, and 2.49-fold when cells were treated with scutellarin at concentrations of 1, 5, and 10 μM, respectively.
Conclusions: This study revealed the cellular protective effects of scutellarin on HaCaT cells. Further studies are warranted to determine the use of scutellarin as a cosmeceutical ingredient.
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KEYWORD
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Scutellarin, Human keratinocytes, Ultraviolet A, Anti-apoptosis, Oxidative stress
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