• Journal of Photoscience
• /
• 제9권2호
• /
• pp.494-496
• /
• 2002

Fluorouracil (FU) is well known to induce discoid lupus-like eruption at the sun exposure sites in Japan. It means the associations of UVB with drug induced DLE. It is still obscure which cytokines are involved in the development of DLE. To address the issue, we established a murine model of FU and UVB-induced discoid lupus and could show the Th1 dominant cytokine profiles in DLE model of TCR $\alpha$ chain KO mice treated with FU and UVB.

• Journal of Photoscience
• /
• 제9권2호
• /
• pp.338-340
• /
• 2002

In broom sorghum, Sorghum bicolor Moench, UV causes anthocyanin synthesis having action peaks in UVA and UVB regions. We previously reported that UV induces anthocyanin synthesis through UVB photoreceptor and phytochrome activated by UV. Furthermore, UVA and UVB amplify phytochrome-induced anthocyanin synthesis (PIAS). Our action- spectroscopic research indicated that a UV -receptor for amplification of PIAS is likely to be the same or same type of UVB photoreceptor for induction of anthocyanin synthesis. UVA-amplification of PIAS can be explained by the action of a cryptic red light signal (CRS), an amplification factor for PIAS produced by a distinct phytochrome-species activated by UVA. We suggest that UVA photoreceptors are not involved in anthocyanin synthesis in the broom sorghum.

• BMB Reports
• /
• 제47권4호
• /
• pp.209-214
• /
• 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.

• 대한약학회:학술대회논문집
• /
• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
• /
• pp.95.2-96
• /
• 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)

• 한국환경보건학회:학술대회논문집
• /
• 한국환경보건학회 2005년도 가을학술대회
• /
• pp.166-168
• /
• 2005

The induction of heme oxygenase-1(HO-1) by ultraviolet(UV) radiation provides a protective defense against oxidative stress, and has been well demonstrated in UVA-irradiated skin, but not UVB. In this study in mice, we show that the UVB(290-320nm) radiation can be attributed to the induction of cutaneous heme oxygenase-1. The expression of HO-1 mRNA was assessed in vivo by the reverse transcription-polymerase chain reaction (RT-PCR) analysis, and HO-1 enzyme activity was measured in microsomal preparation from irradiated mice. The mRNA level of HO-1 increases in liver and skin from 24h to 72h after UVB($3KJ/m^3$) radiation. The results of gene expression were same pattern of HO enzyme activity in skin, but not in liver. HO-1 mRNA in liver resulted in a progressive increase to 96h after UVB radiation, but HO activity in liver increased to 48h. This finding indicates that UVB radiation is an important inducer of HO-1 and increases in HO activity may protect tissues directly or indirectly from oxidative stress.

• Biomolecules & Therapeutics
• /
• 제23권2호
• /
• pp.165-173
• /
• 2015

Most skin damage caused by ultraviolet B (UVB) radiation is owing to the generation of reactive oxygen species. Phytochemicals can act as antioxidants against UVB-induced oxidative stress. This study investigated the protective effects of the flavone galangin against UVB-induced oxidative damage in human keratinocytes. Galangin efficiently scavenged free radicals and reduced UVB-induced damage to cellular macromolecules, such as DNA, lipids, and proteins. Furthermore, galangin rescued cells undergoing apoptosis induced by UVB radiation via recovering mitochondrial polarization and down-regulating apoptotic proteins. These results showed that galangin protects human keratinocytes against UVB radiation-induced cellular damage and apoptosis via its antioxidant effects.

• Biomolecules & Therapeutics
• /
• 제24권3호
• /
• pp.312-319
• /
• 2016

Human skin cells undergo pathophysiological processes via generation of reactive oxygen species (ROS) upon excessive exposure to ultraviolet B (UVB) radiation. This study investigated the ability of hesperidin ($C_{28}H_{34}O_{15}$) to prevent apoptosis due to oxidative stress generated through UVB-induced ROS. Hesperidin significantly scavenged ROS generated by UVB radiation, attenuated the oxidation of cellular macromolecules, established mitochondrial membrane polarization, and prevented the release of cytochrome c into the cytosol. Hesperidin downregulated expression of caspase-9, caspase-3, and Bcl-2-associated X protein, and upregulated expression of B-cell lymphoma 2. Hesperidin absorbed wavelengths of light within the UVB range. In summary, hesperidin shielded human keratinocytes from UVB radiation-induced damage and apoptosis via its antioxidant and UVB absorption properties.

• Environmental Analysis Health and Toxicology
• /
• 제24권4호
• /
• pp.351-357
• /
• 2009

To investigate the alleviative effects of jujube water extract (JWE) on the inflammation and skin barrier damage, both the irradiation of UVB and the application of squalene monohydroperoxide (Sq-OOH) were applied to the back skin of experimental animals for 4 weeks. And at the same time experimental materials were applied topically. Six weeks female SKH-1 hairless mice were divided into five groups (five animals for each group) including normal (N; saline), control (C; UVB+Sq-OOH+saline), vehicle control (VC; UVB+Sq-OOH+vehicle), positive control (PC; UVB+Sq-OOH+0.01% retinoic acid) and experimental (E; UVB+Sq-OOH+JWE) groups. The skin erythema index in the E group was significantly low compared to the C group (p<0.05). Lipid (p<0.05) and water (p<0.01) capacities in the E group were significantly high compared to the C group. In comparison with the C group, E group showed a relatively well preserved lipid lamellae in the epidermis and a relatively much less infiltration of mast cells in the dermis or hypodermis. As for the both absolute and relative weights of the spleen, PC group were significantly higher than the other groups. These results suggest that JWE have a considerably inhibitory effect on the inflammation and the skin barrier damage induced by UVB irradiation and Sq-OOH application.

• Biomolecules & Therapeutics
• /
• 제24권1호
• /
• pp.75-84
• /
• 2016

This study was designed to investigate the cytoprotective effect of rosmarinic acid (RA) on ultraviolet B (UVB)-induced oxidative stress in HaCaT keratinocytes. RA exerted a significant cytoprotective effect by scavenging intracellular ROS induced by UVB. RA also attenuated UVB-induced oxidative macromolecular damage, including protein carbonyl content, DNA strand breaks, and the level of 8-isoprostane. Furthermore, RA increased the expression and activity of superoxide dismutase, catalase, heme oxygenase-1, and their transcription factor Nrf2, which are decreased by UVB radiation. Collectively, these data indicate that RA can provide substantial cytoprotection against the adverse effects of UVB radiation by modulating cellular antioxidant systems, and has potential to be developed as a medical agent for ROS-induced skin diseases.

• Preventive Nutrition and Food Science
• /
• 제20권3호
• /
• pp.162-168
• /
• 2015

Lotus (Nelumbo nucifera Gaertn.) seed is widely used as a traditional medicine in countries of Asia. Among many functions of the lotus seed, one interesting activity is its skin protection from the sunlight and scar. In this study, we focused on the skin protective property of lotus seed tea against ultraviolet B (UVB) irradiation. Two groups of a hairless mouse model, water as control (water group) and lotus seed tea (LST group), were administrated a fluid drink water for six months. After 6 month of administration, UVB exposure was carried out to both groups for another 3 months. During and after the administration, the skin moisture content and the morphological and histopathological analyses through biopsy were carried out. Prior to UVB irradiation, no significant difference was discovered in the skin moisture content for the water group and LST group (P<0.05). However, drastic changes were observed after the UVB treatment. The LST group showed a clear evidence of skin protection compared to the control group (P<0.05). The moisture content, epidermal and horny layer thickness, and protein carbonyl values all revealed that the intake of the lotus seed tea enhanced protection against UVB exposure. As a result, the long-term intake of the lotus seed tea showed the effect of preventing loss of skin moisture, mitigating the formation of abnormal keratinocytes, and contributing to protein oxidation inhibition.