• Environmental Analysis Health and Toxicology
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• 제21권2호
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• pp.165-172
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• 2006

The backs with a hair cut of 6-week-old healthy ICR male mice were once exposed to a dose of $400mJ/cm^2$ UVB. An acute dermal inflammation was observed, and the inflamed skins were almost completely cured after 6 days of the exposure. At 24 hours after exposure, the epidermal keratinocytes showed a cell-membrane damage with the destruction of intercellular junctions, agglutination of tonofilaments within the cytoplasm and nucleus damage. The activity of XO showed a significant increase (p<0.05) in up to 144 hours. The activities of CAT and SOD showed a significant decrease (p<0.05) in up to 96 hours, but they were not significantly different from the normal value at 144 hours. The GST activity was significantly decreased (p<0.01) in up to 96 hours, not so at 24 hours. However, that was not significantly different from the normal value at 144 hours. There was a significant decrease (p<0.01) in the contents of TBARS at 48 and 96 hours, without any significant difference at 144 hours. While the content of GSH was significantly lower (p<0.05) at 24 hours, that was not significantly different thereafter up to 144 hours from the normal value. Therefore, it is assumed that skin damage with a dose of $400mJ/cm^2$ UVB irradiation might be caused by the oxidative stress which was resulted from the unbalance of oxygen fret radical generating and scavenging enzymes.

• Molecular & Cellular Toxicology
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• 제1권2호
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• pp.111-115
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• 2005

Ultraviolet (UV) radiation to mammalian skin is known to alter cellular function via generation of Reactive Oxygen Species (ROS), DNA damage and DNA lesions, such as pyrimidine dimmers and photoproducts, which could lead to DNA mutation if they are not repaired. In this study, we have investigated the reduction of DNA damage and of apoptosis with a particular attention to genetic effect of paeoniflorin in Normal Human Epidermal Keratinocytes (NHEK). After UVB irradiation from $10\;to\;500mJ/cm^{2}$ to NHEK, Mean Tail Moments (MTM) were increased with UVB dose increase. The greatest amount of strand breaks was induced at $500mJ/cm^{2}$ of UVB. Even at the lowest dose of UVB ($10mJ/cm^{2}$), change in MTM was detected (P<0.0001). Pretreated cell with 0.1% paeoniflorin maximally reduced the level of DNA damage to about 21.3%, compared to untreated cell. In the lower concentrations less than 0.01% of paeoniflorin, MTM had a small increase but paeoniflorin still had reductive effects of DNA damage. We measured the apoptosis suppression of paeoniflorin with annexin V flous staining kit. As we observed under the fluorescence microscopy to detect apoptosis in the irradiated cell, the fluorescence intensity was clearly increased in the untreated cell, but decreased in treated cells with paeoniflorin. These results suggest that paeoniflorin reduces the alteration of cell membranes and prevents DNA damage. Therefore, the use of paeoniflorin as a free radical scavenger to reduce the harmful effects of UV lights such as chronic skin damage, wrinkling and skin cancer can be useful to prevent the formation of photooxidants that result in radical damage.

• 생명과학회지
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• 제30권10호
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• pp.867-876
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• 2020

본 연구는 magnolol에 의한 UVB 유도 세포 손상의 복구를 조사하였다. 우리는 약물재배치를 위해 STAT3 기작을 분석하였고, magnolol HDF 세포에서 세포 생존력을 향상시키며, STAT3의 억제제인 것을 확인하였다. IL-6, UVB 및 IFNγ로 처리 된 HDF 세포는 Jak2 및 인산화 된 STAT3 (p-STAT3)의 높은 발현을 나타냈다. Magnolol 의 처리는 UVB 유도 세포에서 Jak2 및 p-STAT3의 발현을 감소시킬 수 있었다. 또한, UVB- 손상된 세포 성장은 용량 의존적 방식으로 재 활성화 및 magnolol 과의 상관 관계가 상당히 증가되었다. UVB 처리 된 HDF 세포에 대한 AG490 (Jak2 억제제) 처리와 비교하여, 세포 증식이 유의하게 증가 하였다. 우리는 AG490 및 magnolol 이 TNF-α 농도를 감소시키는 것을 확인했다. Western blot (단백질 수준)은 오직 magnolol 처리 된 세포에서만 Jak2 및 p-STAT3 발현의 감소를 나타냈고, Jak2, p-STAT3 및 SOCS3의 발현은 또한 magnolol 처리한 세포에서만 증가하였다. 세포를 magnolol 및 ML385 (NRF2 억제제)로 동시 처리시 세포 증식 및 NRF2 발현을 감소시켰다. MMP9의 양은 magnolol 및 ML385 로의 처리에 의해 증가되었다. 종합적으로, 이들 결과는 NRF2, SOCS3, Jak2 및 STAT3의 발현을 조절함으로써 UVB 손상 후 세포를 회복시키는데 있어 magnolol의 가능성을 입증한다.

• 생명과학회지
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• 제20권1호
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• pp.27-32
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• 2010

자외선 B는 반응성 산소종(reactive oxygen species, ROS)의 발생을 유도하고 세포내 항산화 물질의 저장을 방해한다. 후코이단은 L-fucose와 황 에스터기를 포함하는 다당류로서 갈조류의 주요 성분으로 알려져 있다. 본 연구에서는 인간 피부 섬유아세포인 HS68세포에 자외선을 조사하여 산화 스트레스를 유도한 후 후코이단의 보호효과를 확인하고자 하였다. 후코이단의 전처치로 malondialdehyde (MDA)의 양이 용량-의존적으로 감소하였고, 세포내 glutathiopne도 후코이단 $100\;{\mu}g/ml$을 투여하였을 때 후코이단을 투여하지 않고 자외선만 조사한 군에 비하여 21.5% 감소하였다. 후코이단을 10, $100\;{\mu}g/ml$의 용량으로 투여하였을 경우 자외선 B에 의한 ROS 생성이 자외선만 조사하였을 때 보다 각각 40.1%와 68.4%로 유의하게 감소하였다. 세포노화와 관련된 $\beta$-galactosidase의 양성 염색률은 후코이단을 10, $100\;{\mu}g/ml$ 투여하였을 경우 자외선만 조사하였을 때보다 각각 23.1%, 16.4% 감소하였다. 이러한 결과로 미루어 후코이단은 자외선에 의한 산화 스트레스에 대하여 광보호 효과가 있는 것으로 생각된다.

• Journal of Photoscience
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• 제9권2호
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• pp.482-484
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• 2002

UV irradiation activates various intracellular signaling pathways causing cell death in a DNA damage-dependent and an independent manner. As DNA photoproducts, major forms of DNA damage, are maximally formed by UV light at 260-nm, short wavelength UV (UVC) is more harmful than middle wavelength UV (UVB). However, the differences or similarities in responses of DNA damage-independent intracellular signaling molecules to UVB and UVC are not elucidated. We examined activation of signaling molecules towards apoptosis in normal human fibroblastic cells after irradiation with UVB or UVC at a dose generating the equal amount of DNA photoproducts. Both UVB and UVC induced transient phosphorylation of ERK and sustained phosphorylation of p38. Phosphorylation of p53 at Ser15 and at Ser392 residues were also observed, which were inhibited by a phosphoinositide 3-kinase inhibitor, wortmannin. In contrast, an antioxidant N-acetyl-cysteine and a p38 inhibitor SB203580 suppressed only Ser392 phosphorylation, suggesting that UV-induced oxidative stress and p38 activation were involved in the phosphorylation of this site. The apoptic signals such as mitochondrial cytochrome C release and annexin V binding were then observed. Overall, no difference was found in chronological responses of p53, MAPK, and apoptosis between UVB-irradiated and UVC-irradiated cells. These results suggested that DNA damage-independent intracellular signaling molecules similarly responded to UVB and UVC when the equal level of DNA photoproducts were generated.

• Environmental Analysis Health and Toxicology
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• 제23권4호
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• pp.315-323
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• 2008

In this study, the backs with a hair cut of 6-week-old healthy ICR male mice were once exposed to a dose of $400\;mJ/cm^2$ UVB. An acute dermal inflammation was observed, and the certified 100% pure and natural lavender essential oil were applied to the UVB-exposed mice skin twice a day. It was observed that the mice exposed to UVB resulted in an acute inflammation, and when treated with lavender oil the degree of inflammation was much alleviated, and the inflamed skins of both the control and lavender oil-treatment groups were cured almost completely after 6 days of the UVB exposure. At 24 hours after UVB exposure, the epidermal keratinocytes in the control group showed a cell-membrane damage with the destruction of intercellular junctions, agglutination of tonofilaments within the cytoplasm and nucleus damage, while the lavender oil-treatment group had much less cell damage than the control group. While the control group showed a significant increase (p<0.05) in the activity of XO up to 144 hours, the lavender oil-treatment group did not show any significant increase except for 48 hours after the UVB exposure. Both the control and lavender essential oil-treatment groups had a significant decrease in the activities of CAT and SOD up to 96 hours. Particularly, the CAT activity was significantly lower(p<0.05) in the lavender oil-treatment group than the control group up to 48 hours, and higher than the control group at and after 96 hours. The GST activity was significantly decreased in both the control and lavender oil-treatment groups up to 96 hours after the UVB exposure except for the control group at 24 hours, and that of the lavender oil-treatment group was higher than the control group at and after 96 hours. Therefore, it is assumed that the application of the lavender oil to the ultraviolet-damaged mice skin can be effective in treatment for the damaged skin.

• 동의생리병리학회지
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• 제29권1호
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• pp.58-65
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• 2015

This study is designed to investigate the protective effects of fermented Red Ginseng (FRG) against photoaging in vitro and in vivo. UVB was irradiated to the human keratinocyte HaCaT cell and dorsal skin of SKH-1 mice for the induction of photoaging. After treatment of non-fermented red ginseng (NRG), fermented red ginseng (FRG), and fortified fermented red ginseng (FFRG) to the UVB irradiated HaCaT cell, ROS production and activity of MMP-9 were examined by DCFC-DA assay and gelatin zymographic assay respectively. UVB irradiated SKH-1 mice were treated with NRG, FRG, and FFRG via oral(300 mg/Kg B.W./day) and topical($100{\mu}{\ell}/mouse/day$) route.All of NRG, FRG, and FFRG had significantly reduced the intracellular ROS production elicited by UVB, among them FRG slightly more reduced the ROS production than NRG and FFRG. FFRG had slightly more reduced the MMP-9 activity in UVB irradiated HaCaT cells than NRG and FFRG in high dose. Oral and topical treatment of NRG, FRG, and FFRG had decreased the expression of matrix metalloproteinase-2, -3, and -9 in dorsal skin of UVB irradiated mice. Among them, inhibitory effect of FRG on the expression of MMP-2 was apparent. We speculate that FRG has therapeutic potentials on the UVB irradiated photoaging.

• 대한본초학회지
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• 제32권5호
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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.

• 대한화장품학회지
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• 제48권1호
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• pp.33-38
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• 2022

자외선인 ultraviolet B (UVB)는 피부각질세포의 DNA 잔기에 손상을 준다. 특히, DNA의 pyrimidine 잔기 손상인 cyclobutane pyrimidine dimers (CPD)의 형성은 피부 광노화의 대표적인 지표로 여겨진다. 본 연구에서는 피부 각질세포에서 UVB에 의한 DNA 손상을 완화 시키는 소재로 감초추출물(Glycyrrhiza glabra extract, G. glabra extract)의 효능을 확인하였다. 먼저 피부각질세포에서 UVB 의존적으로 CPD형성이 증가하는 것을 확인하였다. 이후 감초추출물에 의해 UVB 유발 CPD 형성이 유의하게 줄어드는 것을 확인할 수 있었다. 추가로 DNA 손상회복 인자의 mRNA 발현이 감초추출물에 의해 증가하는 것도 확인하였다. 결론적으로 본 연구를 통해 감초추출물의 피부각질세포에서의 DNA 보호 효과를 확인할 수 있었다.

• Biomolecules & Therapeutics
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• 제24권3호
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• pp.305-311
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• 2016

Mitochondria-targeted vitamin E (MVE) is designed to accumulate within mitochondria and is applied to decrease mitochondrial oxidative damage. However, the protective effects of MVE in skin cells have not been identified. We investigated the protective effect of MVE against UVB in dermal fibroblasts and immortalized human keratinocyte cell line (HaCaT). In addition, we studied the wound-healing effect of MVE in animal models. We found that MVE increased the proliferation and survival of fibroblasts at low concentration (i.e., nM ranges). In addition, MVE increased collagen production and downregulated matrix metalloproteinase1. MVE also increased the proliferation and survival of HaCaT cells. UVB increased reactive oxygen species (ROS) production in fibroblasts and HaCaT cells, while MVE decreased ROS production at low concentration. In an animal experiment, MVE accelerated wound healing from laser-induced skin damage. These results collectively suggest that low dose MVE protects skin from UVB irradiation. Therefore, MVE can be developed as a cosmetic raw material.