• Journal of Photoscience
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• v.9 no.2
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• pp.433-435
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• 2002

In the present study, we investigated the actions of sphingosine-I-phosphate (SPP) in Mel-Ab melanocytes. We observed the cytoprotective effect of SPP on UVB-induced cell death. Following exposure of cells to UVB, a significant protective effect was seen in cultures pretreated with SPP. Since SPP is well known as a mitogenic agent, it is possible that the mitogenic effect of SPP may contribute to cell survival. Surprisingly, we found that SPP inhibited DNA-synthesis significantly. We were next interested in the regulation of the extracellular signal-regulated protein kinase (ERK) and Akt pathways by SPP. We clearly observed that SPP potently stimulated the phosphorylation of both ERK and Akt against UVB-induced cell death. Based on these results, we conclude that SPP may show its cytoprotective effect through ERK and Akt activation.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.31 no.3 s.52
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• pp.219-236
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• 2005

Glycolic acid, an alpha-hydroxy acid derived from fruit and milk sugars, has been commonly used as a cosmetic ingredient since it was known to have photo-protective, anti-inflammatory effects, and anti-oxidant effect in UV-irradiated skin. However, little has been know about the functional role of glycolic acid on UV-induced skin cell proliferation. It was previously found that glycolic acid inhibited UV-induced skin tumor development in hairless mouse. As a possible mechanism of glycolic acid on the UV-induced skin tumor development, the ability of glycolic acid to inhibit the UVB-induced cell growth and possible mechanisms were investigated. Glycolic acid treatment attenuated the UV-induced cell proliferation and apoptotic cell death in the skin. In vitro study, glycolic acid inhibited the UVB-induced cell growth and apoptotic death through inhibiting caspase-3 activity. These results suggest that glycolic acid may exert the Inhibitory effect on the UVB-induced skin tumor development by regulating cell growth and apoptotic cell death.

• The Korea Journal of Herbology
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• v.32 no.5
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• pp.13-18
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• 2017

Objectives : The aim of this study is to investigate anti-inflammation of Leonurus sibiricus methanol extract against UVB-damage in fibroblast. The skin is continuously exposed to damage from environmental stresses. UV radiation causes a variety of biological effects especially on the skin, including inflammation and photoaging. Methods : In this study, we tried to search for Leonurus sibiricus which exhibit protective activities against UVB-induced cytotoxicity and oxidative cell death, NO and $PGE_2$ production. HS68 cells were exposed to UVB ($120mJ/cm^2$) and treated with various concentrations (0, 0.25, 0.5, 1, 2, 4, $8mg/m{\ell}$) of Leonurus sibiricus methanol extract for additional 24 h. Intracellular reactive oxygen species (ROS) levels generated by UV radiation were detected using a spectrofluorometer after DCF-DA staining. Also, HS68 cells were irradiated with UVB and then treated with Leonurus sibiricus methanol extract for 12 h. The lipid peroxidation was assayed by measuring the levels of 8-isoprostane secreted into the culture medium. Results : UVB-induced cytotoxicity and cell death were effectively suppressed by treatment of Leonurus sibiricus aqueous methanol extracts. Oxidative cell damage was mediated $PGE_2$ in UVB-induced HS68 fibroblast cell, which was significantly inhibited by treatment with Leonurus sibiricus extracts. Also, the protective effect of these extract seemed to be mediated by inhibited intracellular ROS generation and lipid peroxidation in dose-dependent manner. Conclusion : These results suggest that Leonurus sibiricus aqueous methanol extracts may have anti-aging effects new functional materials against oxidative UVB stress-mediated skin damages.

• Biomolecules & Therapeutics
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• v.23 no.4
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• pp.357-366
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• 2015

Isorhamnetin (3-methylquercetin) is a flavonoid derived from the fruits of certain medicinal plants. This study investigated the photoprotective properties of isorhamnetin against cell damage and apoptosis resulting from excessive ultraviolet (UV) B exposure in human HaCaT keratinocytes. Isorhamnetin eliminated UVB-induced intracellular reactive oxygen species (ROS) and attenuated the oxidative modification of DNA, lipids, and proteins in response to UVB radiation. Moreover, isorhamnetin repressed UVB-facilitated programmed cell death in the keratinocytes, as evidenced by a reduction in apoptotic body formation, and nuclear fragmentation. Additionally, isorhamnetin suppressed the ability of UVB light to trigger mitochondrial dysfunction. Taken together, these results indicate that isorhamnetin has the potential to protect human keratinocytes against UVB-induced cell damage and death.

• Biomolecules & Therapeutics
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• v.24 no.6
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• pp.616-622
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• 2016

Baicalein (5,6,7-trihydroxy-2-phenyl-chromen-4-one) is a flavone, a type of flavonoid, originally isolated from the roots of Scutellaria baicalensis. This study evaluated the protective effects of baicalein against oxidative damage-mediated apoptosis induced by ultraviolet B (UVB) radiation in a human keratinocyte cell line (HaCaT). Baicalein absorbed light within the wavelength range of UVB. In addition, baicalein decreased the level of intracellular reactive oxygen species (ROS) in response to UVB radiation. Baicalein protected cells against UVB radiation-induced DNA breaks, 8-isoprostane generation and protein modification in HaCaT cells. Furthermore, baicalein suppressed the apoptotic cell death by UVB radiation. These findings suggest that baicalein protected HaCaT cells against UVB radiation-induced cell damage and apoptosis by absorbing UVB radiation and scavenging ROS.

• Journal of Convergence for Information Technology
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• v.11 no.2
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• pp.201-210
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• 2021

This study was carried out to investigate the Fagopyrum esculentum (F. esculentum) extracts and vitexin are as the results of microarray, cell proliferation, cell wound recovery, cell cycle, microphage pattern and protein analysis for damage improvement caused by UVB-induced damage. Microarray results showed that UVB-induced increase in DRAM1, Atg2a and Atg13 genes was reduced in F. esculentum ethanol extract and vitexin. Cell proliferation, wound repair, cell cycle, and microphage patterns were improved in F. esculentum ethanol extract and vitexin, while buckwheat ethanol extract and vitexin decreased in both DRAM1, Beclin-1, and LC3 I/II in the vitexin treatment group and p-mTOR and survivin were all increased in protein analysis. It is thought that it can recover to normal and control autophagy, one of the causes of cell aging caused by UVB, to inhibit and regenerate cell death. F. esculentum ethanol extract and vitexin can be used as a functional cosmetic ingredient.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.41 no.1
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• pp.9-20
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• 2015

Ultraviolet radiation (UV) is a major cause of skin photoaging, and effective UV protecting agents are needed for the skin health and beauty. This study was undertaken to examine the effects of Bambusae caulis in Taeniam extract (BCTE) on UVB-induced cell death, oxidative stress and matrix metalloproteinase 1 (MMP1) expression in cell-based assays. HaCaT human keratinocytes were exposed to UVB in the presence of BCTE at different concentrations and resulting changes in cell viability and biochemical events were determined. The results showed that BCTE enhanced the viabilities of UVB-exposed cells, and attenuated apoptotic events such as cleavage of procaspase 3 to its active form, and the increase of Bax to Bcl-2 ratios. BCTE also attenuated the reactive oxygen generation and lipid peroxidation in cells exposed to UVB. Additionally, it attenuated the expression of matrix metalloproteinase 1 and the phosphorylation of c-Jun N-terminal kinase stimulated by UVB. Conclusively, the present study demonstrated that BCTE pro tected skin cells from the UVB-induced cell death, oxidative stress and MMP1 expression, suggesting its potential use as a cosmetic ingredient mitigating some features of the skin photoaging.

• Journal of Ginseng Research
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• v.36 no.1
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• pp.68-77
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• 2012

In this study, we investigated the protective effects of processed Panax ginseng, sun ginseng (SG) against the UVB-irradiation on epidermal keratinocytes and dermal fibroblasts. Pretreatment of SG in HaCaT keratinocytes and human dermal fibroblasts reduced UVB-induced cell damage as seen by reduced lactate dehydrogenase release. We also found that SG restored the UVB-induced decrease in anti-apoptotic gene expression (bcl-2 and bcl-xL) in these cells, indicating that SG has an anti-apoptotic effect and thus can protect cells from cell death caused by strong UVB radiation. In addition, SG inhibited the excessive expression of c-jun and c-fos gene by the UVB in HeCaT cells and human dermal fibroblasts. We also demonstrated that SG may exert an anti-inflammatory activity by reducing the nitric oxide production and inducible nitric oxide synthase mRNA synthesis in HaCaT keratinocytes and human dermal fibroblasts. This was further supported by its inhibitory effects on the elevated cyclooxygenase-2 and tumor necrosis factor-${\alpha}$ transcription which was induced by UVB-irradiation in HaCaT cells. In addition, SG may have anti-aging property in terms of induction of procollagen gene expression and inhibition of the matrix metalloprotease-1 gene expression caused by UVB-exposure. These findings suggest that SG can be a potential agent that may protect against the dermal cell damage caused by UVB.

• Journal of Photoscience
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• v.9 no.2
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• pp.217-220
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• 2002

Ultraviolet B (UVB) radiation may activate or deteriorate cultured human epidermal melanocytes, depending on the doses and culture conditions. In this study, we examined whether apoptosis of melanocytes can be induced by physiologic doses of UVB irradiation. PI staining for DNA condensation and flow cytometric analyses demonstrated the apoptotic cell death of melanocytes after UVB irradiation. The level of p53 and Bax revealed a dose-dependent increase with increasing dose of UVB, but the level of Bcl-2 remained unchanged. Confocal microscopic examination showed that Bax moved trom a diffuse to a punctate distribution after UVB irradiation. However, there were no changes in the pattern of Bcl-2. We next examined the downstream targets of apoptosis. Our results showed that a precursor form of caspase-3 disappeared with increasing doses of UVB. We also observed cleavage of poly(ADP-ribose) polymerase (PARP) after UVB irradiation. In addition, UVB irradiation resulted in a remarkable activation of c-Jun N-terminal kinase (JNK). These results indicate that UVB may induce apoptosis via JNK activation in human melanocytes.

• Journal of Life Science
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• v.21 no.5
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• pp.753-760
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• 2011

In the present study, the effects of paprika extract and its components including vitamin C, lycopene and beta-carotene on cell death in ultraviolet B (UVB)-exposed HaCaT cells were investigated. The cell viability upon treatment for 24 hr with either paprika extract or vitamin C alone was similar to or greater than that of the untreated control. However, the viability of the cells treated with lycopene or beta-carotene decreased to about 20% of that in the untreated control. When UVB-exposed cells were post-incubated for 24 hr in medium containing paprika extract or vitamin C, cell viability increased in a concentration dependent manner as compared to those post-incubated in a normal growth medium. In contrast, post-incubation of UVB-exposed cells with lycopene or beta-carotene decreased cell viability in a concentration dependent manner as compared to those post-incubated in a normal growth medium. The nuclear fragmentation analysis showed that paprika extract or vitamin C decreases UVB-induced apoptosis. The apoptotic nuclear fragmentation resulting from UVB exposure was also protected by the paprika extract or vitamin C post-incubation. However, the UVB-induced apoptotic nuclear fragmentation of the cells treated with lycopene or beta-carotene increased in a concentration dependent manner. Western blot analysis showed that either paprika extract or vitamin C treatment alone did not significantly change the level of p53 and GADD45 protein. Interestingly, post-incubation of UVB-exposed cells with paprika extract or vitamin C decreased the p53 and GADD45 protein level as compared to those post-incubated in a normal growth medium. In contrast, incubation of UVB-exposed or non-irradiated cells with lycopene or beta-carotene increased the p53 and GADD45 protein levels in a concentration dependent manner as compared to those incubated in a normal growth medium. All these results suggest that paprika extract and vitamin C help the survival of the UVB-exposed cells, while lycopene and beta-carotene potentiate the apoptotic death of UVB-exposed cells, in accordance with the respective changes in p53 and GADD45 protein levels.