• 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 Plant Resources Society of Korea Conference
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• 2023.04a
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• pp.54-54
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• 2023

Nypa fruticans Wurmb (N. fruticans) is a plant that belongs to Araceae and N. fruticans is mainly found in tropical mangrove systems. The parts (leaves, stems, and roots) of N. fruticans are traditionally used for asthma, sore throat, and liver disease. N. fruticans contains flavonoids and polyphenols, which are substances that have inhibitory effects on cancer and oxidant. In previous studies, some pharmaceutical effects of N. fruticans on melanogenesis and inflammation have been reported. The present study is conducted to investigate the effect of the ethyl acetate fraction of N. fruticans (ENF) on oxidative DNA damage and UVB-induced DNA damage. DNA damage response (DDR) pathway is important in research on cancer, apoptosis, and so on. DDR pathways are considered a crucial factor affecting the alleviation of cellular damage. ENF could reduce oxidative DNA damage derived from reactive oxygen species by the Fenton reaction. Also, ENF reduced the intensity of intracellular ROS in the live cell image by DCFDA assay. UVB is known to cause skin and cellular damage, then finally contribute to causing the formation of tumors. As for the strategies of reducing DNA damage by UVB, inhibition of p53, H2AX, and Chk2 can be important indexes to protect the human body from DNA damage. As a result of confirming the protective effect of ENF for UVB damage, MMPs significantly decreased, and the expression of apoptosis-related factors tended to decrease. In conclusion, ENF can provide protective effects against double-stranded DNA break (DSB) caused by oxidative DNA damage and UVB-induced DNA damage. These results are considered to be closely related to the protective effect against radicals based on catechin, epicatechin, and isoquercitrin contained in ENF. Based on these results, it is thought that additional mechanism studies for inhibiting cell damage are needed.

• 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.

• 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.

• Biomolecules & Therapeutics
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• v.23 no.2
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• pp.165-173
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• 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.

• International Journal of Industrial Entomology and Biomaterials
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• v.47 no.2
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• pp.90-98
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• 2023

The human eye, constantly exposed to solar radiation, can be damaged by UV radiation. In particular, ultraviolet B (UVB)-induced damage plays an important role in retinal degeneration and cell aging. In this study, we investigated the protective effects of the methanol extract of Oxya chinensis sinuosa (OCM), an edible insect known for its high protein content (64.2%), and various pharmacological effects, on human retinal pigment epithelial cells. ARPE-19 cells were treated with OCM and subsequently UVB irradiated. Our results showed that OCM effectively attenuates UVB-induced cell damage by reducing MAPK phosphorylation (JNK and p38 MAPK). Additionally, OCM increased the phosphorylation of Akt, and cell cycle regulators, including p21 and p27, in a dose-dependent manner. Moreover, OCM treatment increased ARPE-19 cell proliferation by activating the S6K1/S6 pathway. This study suggests that OCM prevents UVB-induced retinal cell damage by increasing cell proliferation via ROS reduction, suggesting its potential as a functional therapeutic superfood against retinal cell damage.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.48 no.1
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• pp.33-38
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• 2022

Ultraviolet B (UVB) damages DNA residues in skin keratinocytes. In particular, the formation of cyclobutane pyrimidine dimers (CPD), a pyrimidine residue damage in DNA, is considered a representative indicator of skin photoaging. In this study, we confirmed defensive effect of Glycyrrhiza glabra (G. glabra) extract against UVB induced DNA damage. First of all, we confirmed UVB dependent amount of CPD formation in human keratinocyte cell line. UVB induced CPD was decreased by G. glabra extract by dose dependent manner. In addition, it was confirmed that the expression of mRNA of DNA damage recovery factors was increased by G. glabra extract. Consequently, through this study, it was possible to confirm the DNA protection effect of G. glabra extract in skin keratinocytes.

• The Journal of Korean Obstetrics and Gynecology
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• v.24 no.2
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• pp.33-51
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• 2011

Objectives: This study was performed to assess the protective effect of Saengmaek-san (SM) on UVB-induced HaCaT cell damage. Methods: The protective effects of Saengmaek-san(SM) were determined by UVB-induced HaCaT assay. We assessed protective effects of Saengmaek-san (SM) on LDH release and nitrite release from HaCaT. And COX-2, Bcl-2, Bax, $TNF{\alpha}$, c-jun, c-fos, NF-kB, iNOS, Bcl-xL gene expression were determined in HaCaT using real-time PCR method. Results: 1. SM inhibited LDH-release, nitrite production in UVB-exposed HaCaT. 2. SM suppressed the gene expression of COX-2, $TNF{\alpha}$ in UVB-exposed HaCaT. 3. SM increased the gene expression of Bcl-2, Bax, Bcl-xL family protein in UVB-exposed HaCaT. 4. SM suppressed the gene expression of c-jun, c-fos, NF-kB in UVB-exposed HaCaT. Conclusions: The study showed SM inhibited the cell damage in UVB-exposed HaCaT.

• Journal of Life Science
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• v.24 no.2
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• pp.112-117
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• 2014

We investigated the effects of extracts from Rubus coreanus (RC) and Artemisia princeps var. orientalis (AP) on DNA damage response in ultraviolet B (UVB)-exposed HaCaT cells. Cell activity upon treatment for 24 h with RC or AP alone was similar to or greater than that of the nontreated control. When UVB-exposed cells were postincubated for 24 h in medium containing RC or AP, cell activity increased in a concentration-dependent manner. Nuclear fragmentation analysis showed that postincubation with RC or AP decreased UVB-induced apoptosis by about 20% and 15%, respectively, of that in cells postincubated with growth medium. When UVB-exposed cells were postincubated for 24 h in medium containing RC or AP, the level of cyclobutane pyrimidine dimer decreased in a concentration- dependent manner. Western blot analysis showed that treatment of cells not exposed to UVB with RC or AP alone did not significantly change the levels of phospho-p53 and GADD45 protein. Interestingly, when UVB-exposed cells were postincubated for 24 h in medium containing RC or AP, phospho-p53 and GADD45 levels decreased in a concentration dependent manner. Our results suggest that RC and AP extract assist the survival of UVB-exposed cells in parallel with a decrease in levels of UVB-induced DNA damage and damage-response proteins, such as p53 and GADD45.

• Biomedical Science Letters
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• v.22 no.1
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• pp.18-23
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• 2016

Ultraviolet (UV) irradiation induces cellular damage. A variety of cellular responses for repairing cellular damage including DNA damage occur after UV irradiation. During the repair processes, expression and activation of various molecules are regulated depending on the types of cellular damage. Parkin is an E3 ligase and act as a tumor suppressor. Recently, it has been reported that Parkin is involved in the DNA repair process. In the current study, we investigated whether UVB irradiation influences expression of Parkin. Parkin expression transiently decreased after UVB irradiation both at the mRNA and protein levels, but returned to normal levels thereafter. Taken together with cell viability data, Parkin expression is down-regulated during UVB-induced suppression of cell growth and is increased again in accordance with recovery of UVB-induced cell growth inhibition. However, Parkin overexpression or knockdown did not influence UVB-induced cell growth inhibition and recovery. We propose that Parkin could be a useful molecular marker for evaluating conditions of cells after UVB irradiation.