• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.21 no.1
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• pp.70-82
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• 2008

Objective : The purpose of this study is to examine the effects of Baickbujasan(BB) on the skin damage and depigmentation. Method : The inhibition of tyrosinase activity, melanogenesis and cell viability in cultured B16 melanoma cells were measured. In order to test effects of reduction of melanogenesis, B16 F-10 mouse melanoma stem line was employed to extract melanin from cultured cell, where BB was added or not, and was dissolved in alkali for colorimetric analysis. Also, in order to test skin alteration in C57BL/6 after UV irradiation, the animals were grouped into a UV urradiation group and UV irradiation after BB application group. Dopa oxidase tissue staining was excuted to invesitage the change in the distribution of active melanin cell. The distribution of active melanin cell in inner skin of iNOS after damage from UVB irradiation and the manifestation condition of P53 which takes part in natural death of keratinocyte were examined. Result : The results indicate that BB has significant effects on tyrosinase activity, and melanogenesis in vivo test. BB seems to reduce C57BL/6, external dermatological damage, for instance, erythematous papule, eczema, loss of keratinocyte, reduction in pus, and relieves dermatological damages. Conclusion : BB can be applied externally for UV protection and depigmentation.

• Journal of Photoscience
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• v.9 no.2
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• pp.229-232
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• 2002

There are two distinct UV-responsive signaling pathways in UV-irradiated mammalian cells, i.e., the DNA damage-dependent and -independent pathways. The former occurs in nucleus and results in growth arrest and apoptosis via post-translational modification of p53. The latter is initiated by oxidative stress and/or by damages in cell membrane or cytoplasm, which activate signaling cascade through intracellular molecules including mitogen activated protein kinases (MAPK). In normal human fibroblastic cells, all of MAPK family members, extracellular signal-related kinases (ERK), c-Jun N-terminal kinases (JNK) and p38, were rapidly phosphorylated following UV-irradiation. ERK phosphorylation was suppressed by an inhibitor of receptor tyrosine kinases (RTK). As ERK usually responds to mitogenic stimuli from RTK ligands, UV-induced ERK phosphorylation may be linked to the proliferation of survived cells. In contrast, phosphorylation of JNK and p38, as well as apoptosis, were modulated by the level of UV-generated oxidative stress Therefore, JNK and p38 may take part in oxidative stress-mediated apoptosis. Phosphorylation of p53 at Ser and Thr residues are essential for stabilization and activation of p53. Among several sites reported, we confirmed phosphorylation at Ser-15 and Ser-392 after UV-irradiation. Both of these were inhibited by a phosphoinositide 3-kinase inhibitor, presumably due to the shutdown of signals from DNA damage to p53. Phosphorylation at Ser-392 was also sensitive to an antioxidant and a p38 inhibitor, suggesting that Ser-392 of p53 is one of the possible points where DNA damage-dependent and -independent apoptic signals merge. Thus, MAPK pathway links UV-induced intracellular signals to the nuclear responses and modifies DNA damage-dependent cellular outcome, resulting in the determination of cell death.

• International Journal of Molecular Medicine
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• v.44 no.5
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• pp.1641-1652
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• 2019

Conditioned media from various sources comprise numerous growth factors and cytokines and are known to promote the regeneration of damaged tissues. Among these, natural killer cell conditioned medium (NK-CdM) has been shown to stimulate collagen synthesis and the migration of fibroblasts during the wound healing process. With a long-term aim of developing a treatment for skin photoaging, the ability of NK-CdM to prevent ultraviolet-B (UV-B) damage was assessed in neonatal human dermal fibroblasts (NHDFs) and an in vitro reconstructed skin model. The factors present in NK-CdM were profiled using an antibody array analysis. Protein and mRNA levels in UV-B exposed NHDFs treated with NK-CdM were measured by western blotting and quantitative reverse transcription-PCR, respectively. The total antioxidant capacity of NK-CdM was determined to assess its ability to suppress reactive oxygen species. The anti-photoaging effect of NK-CdM was also assessed in a 3D reconstituted human full skin model. NK-CdM induced proliferation of UV-B-treated NHDFs, increased procollagen expression, and decreased matrix metalloproteinase (MMP)-1 expression. NK-CdM also exhibited a potent antioxidant activity as measured by the total antioxidant capacity. NK-CdM inhibited UV-B-induced collagen degradation by inactivating MAPK signaling. NK-CdM also elicited potential anti-wrinkle effects by inhibiting the UV-B-induced increase in MMP-1 expression levels in a 3D reconstituted human full skin model. Taken together, the suppression of both UV-B-induced MMP-1 expression and JNK activation by NK-CdM suggests NK-CdM as a possible candidate anti-skin aging agent.

• Journal of Physiology & Pathology in Korean Medicine
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• v.24 no.6
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• pp.950-955
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• 2010

In this study, we prepared CheonJeongKiBo-Dan(7 oriental medicinal plants, 7OMP: Astragalus Membranaceus root, Panax Ginseng root, Glycyrrhiza Glabra (licorice) root, Schizandra Chinensis fruit, Polygonatum Odoratum, Rehmannia Glutinosa root, Paeonia Albiflora root) by extracting them in one reactor and studied its efficacies on skin. UV irradiation has been suggested as a major cause of photoaging in skin. In order to investigate protective effects against UV-B induced cellular damage, 7OMP was extracted with 70% ethanol and dissolved in DMSO. The protective effect was detected by MTT assay, reactive oxygen species (ROS) generation, phosphorylation of ATR and p53 in human dermal fibroblast cell system after UV-B irradiation. 7OMP reduced UV-B-induced cellular damage in HDFs cells, and inhibited ROS generation. UV-B-induced toxicity accompanying ROS production and the resultant DNA damage are responsible for activation of ATR, p53 and Bad. In this study, 7OMP hampered phosphorylations of ATR and p53 in human dermal fibroblasts. Therefore, 7OMP may be protective against UV-induced skin photoaging.

• Molecular & Cellular Toxicology
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• v.1 no.2
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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.

• International Journal of Oral Biology
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• v.45 no.4
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• pp.179-189
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• 2020

Green tea polyphenol (-)-epigallocatechin-3-gallate (EGCG) is a potent antioxidant with protective effects against neurotoxicity. However, it is currently unclear whether EGCG protects neuronal cells against radiation-induced damage. Therefore, the objective of this study was to investigate the effects of EGCG on ultraviolet (UV)-induced oxidative stress and apoptosis in PC12 cells. The effects of UV irradiation included apoptotic cell death, which was associated with DNA fragmentation, reactive oxygen species (ROS) production, enhanced caspase-3 and caspase-9 activity, and poly (ADP-ribose) polymerase cleavage. UV irradiation also increased the Bax/Bcl-2 ratio and mitochondrial pathway-associated cytochrome c expression. However, pretreatment with EGCG before UV exposure markedly decreased UV-induced DNA fragmentation and ROS production. Furthermore, the UV irradiation-induced increase in Bax/Bcl-2 ratio, cytochrome c upregulation, and caspase-3 and caspase-9 activation were each ameliorated by EGCG pretreatment. Additionally, EGCG suppressed UV-induced phosphorylation of p38 and rescued UV-downregulated phosphorylation of ERK. Taken together, these results suggest that EGCG prevents UV irradiation-induced apoptosis in PC12 cells by scavenging ROS and inhibiting the mitochondrial pathways known to play a crucial role in apoptosis. In addition, EGCG inhibits UV-induced apoptosis via JNK inactivation and ERK activation in PC12 cells. Thus, EGCG represents a potential neuroprotective agent that could be applied to prevent neuronal cell death induced by UV irradiation.

• International Journal of Oral Biology
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• v.36 no.3
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• pp.149-154
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• 2011

In the present study, total methanol extracts prepared from Alpinia katsumadai showed significant protective effects against the oxidative stress induced by hydrogen peroxide, UV-C or ${\gamma}$-ray irradiation. These protective effects were substantially increased by treatment with 20~100 ${\mu}g$/ml of the extract. The A. katsumadai total methanol preparation was further fractionated into n-hexane, dichloromethane, ethylacetate, n-butanol and water fractions. Among these five fractions, the ethylacetate and butanol fractions of A. katsumadai showed the strongest protective effects against oxidative stress induced by UV-C and ${\gamma}$-ray irradiation. These fractions also showed high DPPH radical scavenging and lipid peroxidation inhibitory activities. In addition, both fractions displayed cell proliferation activation effects, as evidenced by significant increases in colony formation. Our current data thus suggest that the mechanisms underlying the protective effects of A. katsumadai against oxidative damage may include radical scavenging, protection against cell membrane damage and stimulation of cell proliferation.

• Journal of Photoscience
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• v.9 no.2
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• pp.454-456
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• 2002

It is important to determine the action spectrum of UV-B radiation contained in the sunlight to estimate the risk of skin cancer. We have investigated action spectra for induction of apoptosis and reproductive cell death in L5178Y cells using the Okazaki Large Spectrograph at NIBB. L5178Y cells were exposed to light at different wavelengths in UV-B or UV-A region. Frequencies of apoptosis induction and reproductive cell death were determined by counting cells with chromatin condensation, and by the colony formation assay, respectively. The measured sensitivity spectra for the two end-points were in very good agreement. Sensitivity decreased steeply with increase of wavelength in UV-B region and remains nearly constant in UV-A region. The action spectra were also slightly steeper than that for the minimum erythematic dose (MED), but very similar to the light absorption spectrum of DNA in UV-B region. On the other hand, the spectra for both endpoints were similar to MED spectrum but not DNA spectrum in the UV-A region. Also different time-course and morphological difference of apoptosis were found between UV-B (long time, fragmentation) and UV-A (short time, shrinkage) region. These results suggest that DNA damage induced by UV-B light triggers apoptosis and reproductive cell death, but other damaged targets (membrane, protein and so on) trigger these effects in UV-A region.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.7
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• pp.801-808
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• 2017

The present study investigated the protective effects of Bifidobacterium bifidum culture supernatants (BbSC) and intracellular cell-free extracts (BbICFE) on human dermal fibroblasts (HDFs) against ultraviolet-B (UV-B) irradiation. HDFs were treated with UV-B, UV-B+BbCS, and UV-B+BbICFE. Treatment of UV-B-irradiated HDFs with BbCS and BbICFE significantly increased cell viability compared to UV-B-irradiated HDFs. BbCS treatment reduced senescence in HDFs by approximately 40.0%. Moreover, sub-G1 phase was significantly reduced in BbCS- and BbICFE-treated HDFs (3.3% and 4.5%, respectively). The effect of UV-B on oxidative damage of HDFs was measured by dichlorofluorescin diacetate. Fluorescence intensity significantly increased in UV-B-irradiated HDFs. Inhibition of cellular reactive oxygen species in HDFs treated with 0.01% BbCS was the highest at 34.1%. Levels of p21 and p53 protein expression induced by UV-B irradiation were reduced by treatment with BbCS and BbICFE (47.0% and 35.6%, respectively). These results show that BbCS and BbICFE reduce UV-B-induced cellular senescence and apoptosis in HDFs. Thus, BbCS and BbICFE can be used as potential agents for protection of UV-B-induced skin cell damage.

• BMB Reports
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• v.40 no.6
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• pp.966-972
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• 2007

Pituitary tumor transforming gene (PTTG1) is widely detected in many tumors. Increasing evidence reveals that PTTG1 is associated with cell proliferation, cellular transformation and apoptosis. However, the functions of PTTG1, especially its role in DNA damage-induced apoptosis, remain largely unclear. In this report, we used UV irradiation to induce apoptosis in HeLa cells to examine the role of PTTG1 in UV-induced apoptosis by RNAi-mediated knockdown and overexpression of PTTG1. RNAi-mediated knockdown of PTTG1 expression increased and overexpression of PTTG1 decreased the UV-induced apoptosis. Furthermore, UV irradiation decreased PTTG1 mRNA and protein expression. These effects were found to be mediated by JNK pathway. Therefore, PTTG1 had an important anti-apoptotic role in UV-induced apoptosis and this role was mediated by JNK pathway. These results may provide important information for understanding the exact role and the regulation mechanism of PTTG1 in UV-induced apoptosis.