• Korean Journal of Food Science and Technology
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• v.52 no.5
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• pp.467-475
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• 2020

Ultraviolet radiation is a major cause of photoaging, characterized by wrinkle formation and skin dehydration. Mojaban (Sargassum fulvellum), belonging to the brown algae of the Sargassaceae family, exerts anti-inflammatory, antioxidant, and anti-atopic activities. Particularly, Mojaban extract alleviated ultraviolet B (UVB)-induced inflammatory responses in human keratinocytes and BALB/c mice. Here, the dorsal skin of hairless mice was exposed to UVB for photoaging. The mice were administrated 300 mg/kg Mojaban extract (S. fulvellum extract; SFE) daily. Phenotypically, SFE reduced wrinkle formation and epidermal thickness and increased skin elasticity. SFE increased hydroxyproline content by upregulating the expression of collagen-related genes and downregulating matrix metalloproteinase expression. Furthermore, SFE increased skin moisture content and inhibited transepidermal water loss. SFE upregulated the expression of involucrin, loricrin, and transglutaminase for cornified envelope formation as well as the expression of filaggrin and caspase-14 for natural moisturizing factors. Collectively, SFE may be employed as a nutraceutical ingredient for anti-photoaging.

• BMB Reports
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• v.47 no.4
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• pp.209-214
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• 2014

Ultraviolet B (UVB) radiation induces the production of reactive oxygen species (ROS) that promote apoptotic cell death. We showed that cytosolic $NADP^+$-dependent isocitrate dehydrogenase (IDPc) plays an essential role in the control of cellular redox balance and defense against oxidative damage, by supplying NADPH for antioxidant systems. In this study, we demonstrated that knockdown of IDPc expression by RNA interference enhances UVB-induced apoptosis of immortalized human HaCaT keratinocytes. This effect manifested as DNA fragmentation, changes in cellular redox status, mitochondrial dysfunction, and modulation of apoptotic marker expression. Based on our findings, we suggest that attenuation of IDPc expression may protect skin from UVB-mediated damage, by inducing the apoptosis of UV-damaged cells.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.95.2-96
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• 2003

Ultraviolet B (UVB) is known to induce apoptosis in human melanocytes. Here we show the cytoprotective effect of sphingosine-1-phosphate (S1P) against UVB-induced apoptosis. We also show that UVB-induced apoptosis of melanocytes is mediated by caspase-3 activation and poly(ADP-ribose) polymerase (PARP) cleavage, and that S1P prevents apoptosis by inhibiting this apoptotic pathway. We further investigated three major subfamilies of mitogen-activated protein (MAP) kinases and the Akt pathway after UVB irradiation. (omitted)

• ALGAE
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• v.32 no.4
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• pp.379-388
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• 2017

In the present study, we enhanced the phenolic content of 70% ethanol extracts of Spirogyra sp. (SPE, $260.47{\pm}5.21$ gallic acid equivalent $[GAE]mg\;g^{-1}$), 2.97 times to $774.24{\pm}2.61GAE\;mg\;g^{-1}$ in the ethyl acetate fraction of SPE (SPEE). SPEE was evaluated for its antiradical activity in online high-performance liquid chromatography-ABTS analysis, and the peaks with the highest antiradical activities were identified as gallic acid derivatives containing gallic acid, methyl gallate, and ethyl gallate. Isolation of ethyl gallate from Spirogyra sp. was performed for the first time in this study. In ultraviolet B (UVB)-irradiated keratinocytes (HaCaT cells), SPEE improved cell viability by 8.22%, and 23.33% and reduced accumulation of cells in the sub-$G_1$ phase by 20.53%, and 32.11% at the concentrations of 50 and $100{\mu}g\;mL^{-1}$, respectively. Furthermore, SPEE (50 and $100{\mu}g\;mL^{-1}$) reduced reactive oxygen species generation in UVB-irradiated zebrafish by 66.67% and 77.78%. This study suggests a protective activity of gallic acid and its derivatives from Spirogyra sp. against UVB-induced stress responses in both in vitro and in vivo models, suggesting a potential use of SPEE in photoprotection.

• Journal of Life Science
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• v.29 no.12
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• pp.1321-1328
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• 2019

Intermediate-wavelength solar radiation, also known as ultraviolet B (UVB: 290-320 nm) radiation, may cause premature aging and oxidative damage-dependent skin cancer in humans. UVB-induced formation of reactive oxygen species (ROS)-often a consequence of excessive exposure to these rays-could activate matrix metalloproteinases (MMPs) such as MMP-1 and MMP-3. These enzymes break down type I collagen in human fibroblasts. In this study, we assessed the antioxidant and anti-aging effects of ethyl acetate extract of blueberry (EEB). An antioxidant test in blueberries evaluated ROS production using CCD-986sk cells and DPPH assay. In order to evaluate the anti-wrinkle efficacy of blueberries, the MMP-1 production and type 1 procollagen synthesis evaluated and the expression of MMP 1, 3 were tested through Western blot and RT- PCR. EEB exhibited 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging activity and reduced the production of UVB-induced ROS. Also, EEB inhibited UVB-induced processes associated with photoaging and skin cancer, such as reduction in procollagen production and increase in MMP-1 production. More precisely, EEB (50 ㎍/ml) markedly suppressed mRNA and protein levels of MMP-1 and -3. The anti-aging effects are attributable to the antioxidant activity of EEB. These findings indicate that EEB has a protective effect against UVB-induced aging in human fibroblast cells by regulating the levels of type-1 procollagen, MMP-1, and MMP-3.

• Journal of Life Science
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• v.20 no.1
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• pp.27-32
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• 2010

Ultraviolet-B (UVB) radiation induces the formation of reactive oxygen species (ROS) and depletes stores of cellular antioxidants. Fucoidan, polysaccharides containing L-fucose and sulfate ester groups, are constituents of brown algae. In this study, the protective effects of fucoidan on UVB-induced oxidative stress in cultured human skin fibroblast HS68 cells were assessed. Pretreatment with fucoidan significantly reduced malondialdehyde (MDA) content in a dose-dependent manner. With fucoidan pretreatment at a dose of $100\;{\mu}g/ml$, the level of intracellular glutathione was increased by 21.5%, compared to UVB irradiation alone. Fucoidan significantly reduced UVB-induced ROS generation by 40.1% and 68.4% at 10 and $100\;{\mu}g/ml$, respectively, compared to UVB irradiation alone. The positive staining rates of senescence-associated $\beta$-galactosidase were reduced by 23.1% and 16.4% with 10 and $100\;{\mu}g/ml$ of fucoidan, compared to UVB irradiation alone. Fucoidan may exert a photoprotective effect against UVB radiation-induced oxidative stress.

• Journal of Radiation Protection and Research
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• v.32 no.2
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• pp.65-69
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• 2007

The effects of bamboo (Phyllostachys nigra var. henenis Strapf) leaf extract (BLE) on the changes of ultraviolet (UV) light B radiation-induced apoptotic sunburn cell (SBC) and epidermal ATPase-positive dendritic cell (DC) in SKH1-hr or ICR mouse were investigated. The mice were treated with UVB ($200mJ/cm^2$) and were sacrificed 24 hours later. BLE (50 mg/kg of body weight) or vehicle (saline) was given i.p. at 36 and 12 hours before irradiation, and 30 minutes after irradiation. BLE cream (0.2%) or cream base (vehicle) was also topically treated at 24 hours and 15 minutes before irradiation, and immediately after irradiation. The skin of SKH1-hr mouse prepared from the back of untreated mice exhibited about 0.3 SBC/cm length of epidermis, and 24 hours after UV irradiation, the applied areas show an increased number of SBCs. But the frequency of UVB-induced SBC formation was significantly reduced by intraperitoneal injection (59.0%) and topical application (31.8%) of BLE extract. The numbers of DC in normal ICR mouse were $628.00{\pm}51.56\;or\;663.20{\pm}62.58\;per\;mm^2$ of ear epidermis. By 1 day after UVB treatment, the number of ATPase-positive $cells/mm^2$ were decreased by 39.0% or 27.1% in i.p. or topical application group with vehicle. The frequency of UVB ($200mJ/cm^2$)-induced DC decrease was reduced by treatment of BLE as 25.7% in i.p. group and 3.2% in topical application group compared with the irradiation control group. The results presented herein that BLE administration could reduce the extent of skin damages produced by UVB.

• Journal of Photoscience
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• v.9 no.2
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• pp.162-165
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• 2002

Rice is widely cultivated in various regions throughout Asia. Over a five-year period, we investigated the effects of supplemental UVB radiation on the growth and yield of Japanese rice cultivars in the field. The findings of that study indicated that supplemental UVB radiation has inhibitory effects on the growth and grain development. Furthermore, we investigated the sensitivity to UVB radiation of rice cultivars of 5 Asian rice ecotypes, and found that rice cultivars vary widely in UVB sensitivity. The aim of our study is improving UVB resistance in plants by bioengineering or breeding programs. In order to make it, there is need to find the molecular origin of the sensitivity to UVB. Cyclobutane pyrimidine dimer (CPD) is major UV-induced DNA lesions. Plants possess two mechanisms to cope with such DNA damage. The first is the accumulation of UV-absorbing compounds. Our previous data showed that the steady-state CPD levels in leaves of rice grown under chronic radiation in any culture were not so greatly influenced by the increased UV-absorbing compounds content, although there was a significant positive correlation between the CPD levels induced by challenge UVB exposure and the UV-absorbing compounds content. The other is the repair of DNA damage. Photorepair is the major pathway in plants for repairing CPD. We found that the sensitivity to UVB could seriously correlate with the low ability in CPD photorepair in rice plants. These results suggest that photo lyase might be an excellent candidate for restoration by way of selective breeding or engineering in rice.

• Journal of Ginseng Research
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• v.30 no.4
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• pp.194-198
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• 2006

The effects of red ginseng (RG) on the changes of ultraviolet (UV) light B radiation-induced apoptotic sun-burn cell (SBC) and epidermal ATPase-positive dendritic cell (DC) in SKH 1-hr or ICR mouse were investigated. The mice were treated with UVB ($200mJ/cm^2$) and were sacrificed 24 hours later. RG (50 mg/kg of body weight) or vehicle (saline) was given i.p. at 36 and 12 hours before irradiation, and 30 minutes after irradiation. RG cream (0.2%) or cream base (vehicle) was also topically treated at 24 hours and 15 minutes before irradiation, and immediately after irradiation. The skin of SKH 1-hr mouse prepared from the back of untreated mice exhibited about 0.3 SBC/cm length of epidermis, and 24 hours after UV irradiation, the applied areas show an increased number of SBCs. But the frequency of UVB-induced SBC formation was significantly reduced by intraperitoneal injection of RG extract. The numbers of DC in normal ICR mouse were $628.00{\pm}51.56\;or\;663.20{\pm}62.58\;per\;mm^2$ of ear epidermis. By 1 day after UVB treatment, the number of ATPase-positive $cells/mm^2$ were decreased by 39.0% or 27.1% in i.p. or topical application group with vehicle. The frequency of UVB ($200mJ/cm^2$)-induced DC decrease was reduced by treatment of RG as 31.3% in i.p. group and 22.4% in topical application group compared with the irradiation control group. The results presented herein that RG administration could reduce the extent of skill damages produced by UVB.

• Molecules and Cells
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• v.42 no.2
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• pp.151-160
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• 2019

Ultraviolet (UV) radiation of the sunlight, especially UVA and UVB, is the primary environmental cause of skin damage, including topical inflammation, premature skin aging, and skin cancer. Previous reports show that activation of nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$) in human skin fibroblasts and keratinocytes after UV exposure induces the expression and release of proinflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$), and subsequently leads to the production of matrix metalloproteases (MMPs) and growth factor basic fibroblast growth factor (bFGF). Here, we demonstrated that TNFR2-SKEE and TNFR2-SKE, oligopeptides from TNF receptor-associated factor 2 (TRAF2)-binding site of TNF receptor 2 (TNFR2), strongly inhibited the interaction of TNFR1 as well as TNFR2 with TRAF2. In particular, TNFR2-SKE suppressed UVB- or $TNF-{\alpha}$-induced nuclear translocalization of activated $NF-{\kappa}B$ in mouse fibroblasts. It decreased the expression of bFGF, MMPs, and COX2, which were upregulated by $TNF-{\alpha}$, and increased procollagen production, which was reduced by $TNF-{\alpha}$. Furthermore, TNFR2-SKE inhibited the UVB-induced proliferation of keratinocytes and melanocytes in the mouse skin and the infiltration of immune cells into inflamed tissues. These results suggest that TNFR2-SKE may possess the clinical potency to alleviate UV-induced photoaging in human skin.