Abstract
BackgroundThis study examines the cellular protective effects of scutellarin on HaCaT cells in which oxidative stress was induced by ultraviolet A (UVA).MethodsCell 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.ResultsAlthough 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.ConclusionsThis 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.
Highlights
This study examines the cellular protective effects of scutellarin on HaCaT cells in which oxidative stress was induced by ultraviolet A (UVA)
Changes in lipid peroxidation due to scutellarin in HaCaT cells irradiated with UVA This experiment confirmed the inhibitive effect of scutellarin in intracellular lipid peroxidation induced by UVA
When HaCaT cells were irradiated by UVA (10 J/cm2), lipid peroxidation increased 3.63 times more than that in the non-treated control group, whereas it decreased in a concentration-dependent manner, with values that were 2.06, 1.38, and 0.97 times greater due to increasing concentrations of scutellarin (1, 5, and 10 μM, respectively) (Fig. 3)
Summary
This study examines the cellular protective effects of scutellarin on HaCaT cells in which oxidative stress was induced by ultraviolet A (UVA). As the outermost wall of the human body, skin is damaged by the primary invasion from the external environment to cause aging by oxidative stress from UVA (Gibbs et al 2014; Giacomoni and Rein 2001). UVA and UVB cause apoptosis through different signaling pathways in HaCaT cells (Karran and Brem 2016). As they are most closely involved, they are among the subjects of interest in the field of esthetics (Marionnet et al 2014). UV-induced apoptosis activates the cellular tumor antigen p53, while other features determine cell viability and apoptosis, including mitochondrial damages, cytochrome C release, caspase cascade activity through TNF-related apoptosis-inducing receptors, and the balance between apoptosis-inducing proteins such as Bax, Bak, Bid, and anti-apoptosis proteins such as Bcl-2, Bcl-xl, and Bcl-w (Ostling et al 1984)
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