• Applied Microscopy
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• v.38 no.3
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• pp.195-204
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• 2008

This study was intended to identify the effectiveness of Lithospermum erythrorhizon in the UVB-irradiated mouse skin. The C57BL mice were divided into three groups; the control group, the UVB irradiated group(UVB group), and the group treated with Lithospermum erythrorhizon extracts after UVB irradiation(UVB+Le group). 10 mouses were collected and sacrificed at 24 hrs, 48 hrs, 72 hrs, 120 hrs, and 168 hrs, respectively. In the result, the transepidermal water loss (TEWL) was decreased the UVB+Le group than UVB groups by time. At the 168 hrs group was significantly lower(p<0.05). In the result, the melanin value was decreased in the UVB+Le group than UVB group, but meaningless(p>0.05). In the result of erythema index, the UVB+Le group was meaningfully lower at 24 hrs, 48 hrs, and 72 hrs group than UVB group(p<0.05). In the result of scanning electron micrograph observation, the UVB+Le group was allevited swelling than UVB group at the 24 hrs, formation of the scab at the 48 hrs, regular plate shap at the 72 hrs, new keratin observated at the 120 hrs partially, and fine fiber covered epidermis surface at the 168 hrs. In the result of transmission electron micrograph observation, the UVB+Le group was facilitation of increased lamellar bodies and reformation lamellar bodies than UVB group at the all groups. Almost all the structures were recovered at the 160 hrs group. In conclusion, Lithospermum erythrorhizon extracts may recovery on the UVB-irradiated mouse skin.

• Korean Journal of Pharmacognosy
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• v.44 no.4
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• pp.391-396
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• 2013

In this study, we investigated the effects of onion(Allium cepa L.) peel extraction aplication on UVB-induced damage of mouse skin. The male C57BL/6 weeks mice were divided into three groups; the control group(Con), the UVB irradiated group(UVB) and the group treated with onion peel extract after UVB irradiation(UVB+Onion peel). Onion peel extraction were topically treated after UVB irradiation(800 $mJ/cm^2$) to dorsal skin. We were measured TEWL, melanin value, erythema index and histological of mouse skin. In the TEWL, melanin value and erythema index observation, UVB+onion peel group were decreased then in the UVB group and 120 and 168 hr groups were similar to the control group. In the histological observation, UVB+onion peel group were indicated hyperkeratosis then in the UVB. These results showed that onion peel extract as a topical application may have preventive effect against UVB-induced skin damage. Therefore onion peel extract might be good material for UVB-damage skin care.

• Proceedings of the Korean Society of Plant Biotechnology Conference
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• 2004.10a
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• pp.29-34
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• 2004

Reduction in stratospheric ozone layer increases the amount of ultraviolet-B radiation (UVB: 280-320 nm) that reaches the earth ’ s surface. UVB radiationcan damage plants, resulting in decrease in growth and productivity. UVB-augmentation studies have indicated that the sensitivity to UVB radiation in plants varies among the species and cultivars. However. there are no definitive answers for the mechanisms of UVB-resistance in higher plants and for bioengineering design and development of UVB-tolerant plants. We have been studying physiological and biochemical aspects of the effects of UVB radiation on growth and yield of rice COryza sativa LJ. aiming to clarify the mechanism of resistance to UVB radiationin rice. At this meeting. weintroduce our research as followed: (1) supplementary UVB radiation has inhibitory effects on the growth. yield and grain development of rice; (2) UVB sensitivity of rice varies widely among cultivars; (3) among Japanese rice cultivars. Sasanishiki. a leading variety in northeast Japan. is more resistant to UVB. while Norin 1. a progenitor of Sasanishiki. is less resistant; (4)UV-sensitive Norin 1 cultivar is deficient in photorepair of UVB-induced cyclobutane pyrimidine dimer (CPD). and this deficiency results from one amino acid residue alteration of CPD photolyase. These results suggest that spontaneously occurring mutation in CPD photolyase gene could lead to difference in UVB sensitivity in rice. and that CPD photolyase might be a useful target for improving UVB-sensitivity in rice by selective breeding or bioengineering of UVB-tolerant rice.

• The Journal of Korean Obstetrics and Gynecology
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• v.24 no.4
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• pp.31-49
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• 2011

Objectives: This study was performed to assess the protective effect of Polygonum multiflorum(PM) on UVB-irradiated HaCaT Keratinocytes damage. Methods: The protective effects of Polygonum multiflorum(PM) were determined by UVB-irradiated HaCaT assay. We assessed protective effects of Polygonum multiflorum(PM) on LDH release and nitrite production from HaCaT. COX-2, Bcl-2, Bax, $TNF{\alpha}$, c-jun, c-fos, NF-${\kappa}B$, iNOS, Bcl-xL gene expression were determined in HaCaT using real-time PCR method. Results: 1. PM inhibited LDH Release in UVB-irradiated HaCaT Keratinocytes. 2. PM inhibited Nitrite Production in UVB-irradiated HaCaT Keratinocytes. 3. PM suppressed the Gene Expression of COX-2 in UVB-irradiated HaCaT Keratinocytes. 4. PM increased the Gene Expression of Bcl-2 in UVB-irradiated HaCaT Keratinocytes. 5. PM didn't increase the Gene Expression of Bax in UVB-irradiated HaCaT Keratinocytes. 6. PM suppressed the Gene Expression of $TNF{\alpha}$ in UVB-irradiated HaCaT Keratinocytes. 7. PM suppressed the Gene Expression of c-jun in UVB-irradiated HaCaT Keratinocytes. 8. PM suppressed the Gene Expression of c-fos in UVB-irradiated HaCaT Keratinocytes. 9. PM suppressed the Gene Expression of NF-${\kappa}B$ in UVB-irradiated HaCaT Keratinocytes. 10. PM suppressed the Gene Expression of i-NOS in UVB-irradiated HaCaT Keratinocytes. 11. PM didn't increase the Gene Expression of Bcl-xL in UVB-irradiated HaCaT Keratinocytes Conclusions: In conclusion, these results suggest that PM inhibited the cell damage in UVB-irradiated HaCaT.

• Environmental Mutagens and Carcinogens
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• v.17 no.1
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• pp.17-22
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• 1997

We observed the frequency of chromosome aberrations induced by UVB irradiations, and the suppressing effect of tannic acid on chromosome aberrations induced by UVB irradiations in CHL cells, which is a phenolic compound, a hydrolysate of tannin and a components of green tea. UVB doses used for the frequency of chromosome aberrations were from 0.2 to 1.6 KJ/m$^2$ and tannic acid concentrations were from 1.16 $\mu$g/ml to 37.50 $\mu$g/ml. For the observation of suppressing effect of tannic acid on UVB-induced chromosome aberrations, UVB dose was 1.6 KJ/m$^2$ and tannic acid concentrations were 1.0, 2.0, 4.0 $\mu$g/ml. In our study, tannic acid was treated for 24 hours in CHL, cells after UVB irradiation without S9 mix or for 6 hours with S9 mix. From this study, we obtained the following results : (1) The frequency of chromosome aberrations UVB induced were dose-dependently increased. (2) The tannic acid did not induce chromosome aberrations in cultured Chinese hamster cells. (3) UVB-induced chromosome aberrations were suppressed by tannic acid at every concentration from 1.0 $\mu$g/ml to 4.0 $\mu$g/ml with or without metabolic activation. These results suggest that the tannic acid acts as an inhibitor to UVB-induced clastogenicity of the cultured cell.

• Nutrition Research and Practice
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• v.8 no.4
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• pp.398-403
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• 2014

BACKGROUND/OBJECTIVES: Ultraviolet B (UVB) irradiation on skin can induce production of reactive oxygen species (ROS), which cause expression of matrix metalloproteinases (MMPs) and collagen degradation. Thus, chronic exposure of skin to UVB irradiation leads to histological changes consistent with aging, such as wrinkling, abnormal pigmentation, and loss of elasticity. We investigated the protective effect of the standardized green tea seed extract (GSE) on UVB-induced skin photoaging in hairless mice. MATERIALS/METHODS: Skin photoaging was induced by UVB irradiation on the back of Skh-1 hairless mice three times per week and UVB irradiation was performed for 10 weeks. Mice were divided into six groups; normal control, UVB irradiated control group, positive control (UVB + dietary supplement of vitamin C 100 mg/kg), GSE 10 mg/kg (UVB + dietary supplement of GSE 10 mg/kg), GSE 100 mg/kg (UVB + dietary supplement of GSE 100 mg/kg), and GSE 200 mg/kg (UVB + dietary supplement of GSE 200 mg/kg). RESULTS: The dietary supplement GSE attenuated UVB irradiation-induced wrinkle formation and the decrease in density of dermal collagen fiber. In addition, results of the antioxidant analysis showed that GSE induced a significant increase in antioxidant enzyme activity compared with the UVB irradiation control group. Dietary supplementation with GSE 200 mg/kg resulted in a significant decrease in expression of MMP-1, MMP-3, and MMP-9 and an increase in expression of TIMP and type-1 collagen. CONCLUSIONS: Findings of this study suggest that dietary supplement GSE could be useful in attenuation of UVB irradiation-induced skin photoaging and wrinkle formation due to regulation of antioxidant defense systems and MMPs expression.

• Archives of Pharmacal Research
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• v.28 no.7
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• pp.784-790
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• 2005

In this study, we evaluate the effects of (-)-epigallocatechin-3-gallate (EGCG) on ultraviolet B(UVB)-irradiated living skin equivalents (LSEs). Histologically, UVB irradiation induced thinning of the LSE epidermis, whereas EGCG treatment led to thickening of the epidermis. Moreover, EGCG treatment protected LSEs against damage and breakdown caused by UVB exposure. Immunohistochemically, UVB-exposed LSEs expressed p53, Fas, and 8-hydroxy-deoxyguanosine (8-OHdG), all of which are associated with apoptosis. However, EGCG treatment reduced the levels of UVB-induced apoptotic markers in the LSEs. In order to determine the signaling pathways induced by UVB, Western blot analysis was performed for both c-Jun $NH_2$-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), which are associated with UVB-induced oxidative stress. UVB activated JNK in the epidermis and dermis of the LSEs, and EGCG treatment reduced the UVB-induced phosphorylation of JNK. In addition, p38 MAPK was also found to have increased in the UVB-exposed LSEs. Also, EGCG reduced levels of the phosphorylation of UVB-induced p38 MAPK. In conclusion, pretreatment with EGCG protects against UVB irradiation via the suppression of JNK and p38 MAPK activation. Our results suggest that EGCG may be useful in the prevention of UVB-induced human skin damage, and LSEs may constitute a potential substitute for animal and human studies.

• 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 Photoscience
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• v.9 no.2
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• pp.201-204
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• 2002

Epidermal cells produce a panel of antioxidants as well as cytokines after UVB irradiation, which counteract reactive oxygen species, however, how these antioxidants might regulate melanogenesis is unclear. An important constituent of the cellular antioxidant buffering system which controls the redox state of proteins is thioredoxin (TRX), a 13-kD protein that catalyzes thiol-disulfide exchange reactions, regulates activation of transcription factors, and possesses several other biological functions similar to cytokines. TRX suppressed the UVB-induced production and secretion of $\alpha$-melanocyte stimulating hormone ($\alpha$-MSH) and of adrenocorticotropic hormone (ACTH), and also suppressed proopiomelanocortin (POMC) mRNA expression by normal human keratinocyte (KC)s. Further, L-cysteine, N-acetyl-cysteine, $\alpha$-tocopheryl ferulate showed suppressive effect on UVB-induced POMC mRNA expression. However, TRX released from UVB-irradiated KCs stimulated melanogenesis by up-regulating MSH receptor expression and its binding activity in melanocyte (MC)s. UVB-induced KC derived cytokines such as IL1, IL6, and ET1 upregulated MSH-receptor binding ability as well as MCl-R mRNA expression in cultured normal human MCs. MCl-R has a tendency to be upregulated by UVB-induced KC-derived cytokines as well as by direct UVB irradiation. These results suggest that antioxidants such as TRX suppresses UVB induction of POMC, but in the case of MCl-R, this gene can be mainly in the trend of upregulation by UVB-induced KC-derived factors including TRX.

• Journal of the Korean Society of Clothing and Textiles
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• v.21 no.4
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• pp.750-756
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• 1997

The purpose of the study was to investigate a transmittance rate of UVB (Ultraviolet B) through summer fabrics and a protection rate of summer fabric from UVB. The subjects were randomly selected 159 fabrics from Korean common summer fabrics. The protection rates of 159 fabrics from UVB were measured by UVB lamp and UVB sensor, and 14 fabrics among these fabrics were selected for an assay of MTT(3-(4, 5-dimethylthiazol-2-yl) -2, 5 -diphenyltetrazolium). The protection rate of fabrics from cell toxicity of UVB was measured by investigating the difference of the amount of cell toxic substance on between fabrics covered with and without HeLa cell The average protection rate of 159 fabrics from UVB was 95.08%. As result findings, three negative correlations were found between: 1) the transmittance rate of UVB and the amount of MTT on fabrics (y=0.0373+0.O0518 x, r=-0.9323, p<0.001); 2) the air permeability of fabrics and the amount of MTT (r: -0.79, p< 0.01); 3) the air permeability of fabrics and the protection rate of fabrics from UVB (r=0.89, p<0.01). However, there was no effect of thickness of fabrics on the protection rate from UVB and the amount of MTT.