scholarly journals Empetrum nigrumvar.japonicumExtract Suppresses Ultraviolet B-Induced Cell Damage via Absorption of Radiation and Inhibition of Oxidative Stress

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Ki Cheon Kim ◽  
Daeshin Kim ◽  
Sang Cheol Kim ◽  
Eunsun Jung ◽  
Deokhoon Park ◽  
...  
Keyword(s):  
Apoptotic Cell ◽  
Cell Damage ◽  
Human Keratinocytes ◽  
Ultraviolet B ◽  
Cellular Damage ◽  
Peroxidation Of Lipids ◽  
Uvb Radiation ◽  
Hacat Keratinocytes ◽  
Dna Strands ◽  
Cellular Components

This study focused on the protective actions ofEmpetrum nigrumagainst ultraviolet B (UVB) radiation in human HaCaT keratinocytes. An ethyl acetate extract ofE. nigrum(ENE) increased cell viability decreased by exposure to UVB rays. ENE also absorbed UVB radiation and scavenged UVB-induced intracellular reactive oxygen species (ROS) in HaCaT keratinocytes. In addition, ENE shielded HaCaT keratinocytes from damage to cellular components (e.g., peroxidation of lipids, modification of proteins, and breakage of DNA strands) following UVB irradiation. Furthermore, ENE protected against UVB-induced apoptotic cell death, as determined by a reduction in the numbers of apoptotic bodies and sub-G1hypodiploid cells, as well as by the recovery of mitochondrial membrane potential. The results of the current study therefore suggest that ENE safeguards human keratinocytes against UVB-induced cellular damage via the absorption of UVB ray and scavenging of UVB-generated ROS.

Ultraviolet B radiation induces cell shrinkage and increases osmolyte transporter mRNA expression and osmolyte uptake in HaCaT keratinocytes

2007 ◽  
Vol 388 (12) ◽  
pp. 1345-1352 ◽  
Author(s):  
Ulrich Warskulat ◽  
Stefanie Brookmann ◽  
Andrea Reinen ◽  
Dieter Häussinger
Keyword(s):  
Mrna Expression ◽  
Cell Line ◽  
Human Keratinocytes ◽  
Ultraviolet B ◽  
Organic Osmolytes ◽  
Mrna Levels ◽  
Hacat Cells ◽  
Uvb Radiation ◽  
Hacat Keratinocytes ◽  
Cell Shrinkage

Abstract We have previously shown that compatible organic osmolytes, such as betaine, myo-inositol and taurine, are part of the stress response of normal human keratinocytes (NHKs) to ultraviolet B (UVB) radiation. In this regard, we tested human HaCaT keratinocytes as a surrogate cell line for NHK. HaCaT cells osmo-dependently express mRNA specific for transport proteins for betaine (BGT-1), myo-inositol (SMIT) and taurine (TAUT). Compared to normoosmotic (305 mosmol/l) controls, which strongly constitutively expressed BGT-1 mRNA, strong induction of SMIT and TAUT mRNA as well as low induction of BGT-1 mRNA expression was observed between 3 and 9 h after hyperosmotic exposure (405 mosmol/l). This expression correlated with an increased osmolyte uptake. Conversely, hypoosmotic (205 mosmol/l) stimulation led to a significant efflux of osmolytes. Exposure to UVB (290–315 nm) radiation induced cell shrinkage which was followed by an upregulation of osmolyte transporter mRNA levels and osmolyte uptake. These results demonstrate that human HaCaT keratinocytes possess an osmolyte strategy including UVB-induced cell shrinkage and following increased osmolyte uptake. However, several differences in osmolyte transporter expression and uptake were noted between NHK and HaCaT cells, indicating that the use of HaCaT cells as a surrogate cell line for NHK has limitations.

scholarly journals UVB protective effects of Sargassum horneri through the regulation of Nrf2 mediated antioxidant mechanism

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Eui Jeong Han ◽  
Seo-Young Kim ◽  
Hee-Jin Han ◽  
Hyun-Soo Kim ◽  
Kil-Nam Kim ◽  
...  
Keyword(s):  
Skin Barrier ◽  
Human Keratinocytes ◽  
Underlying Mechanism ◽  
Ultraviolet B ◽  
Sargassum Horneri ◽  
Cellular Damage ◽  
Protective Effects ◽  
Skin Damage ◽  
Antioxidant Mechanism ◽  
Induced Apoptosis

AbstractThe present study aimed to evaluate the protective effect of a methanol extract of Sargassum horneri (SHM), which contains 6-hydroxy-4,4,7a-trimethyl-5,6,7,7a-tetrahydrobenzofuran-2(4H)-one (HTT) and apo-9′-fucoxanthinone, against ultraviolet B (UVB)-induced cellular damage in human keratinocytes and its underlying mechanism. SHM significantly improved cell viability of UVB-exposed human keratinocytes by reducing the generation of intracellular reactive oxygen species (ROS). Moreover, SHM inhibited UVB exposure-induced apoptosis by reducing the formation of apoptotic bodies and the populations of the sub-G1 hypodiploid cells and the early apoptotic cells by modulating the expression of the anti- and pro-apoptotic molecules, Bcl-2 and Bax, respectively. Furthermore, SHM inhibited NF-κB p65 activation by inducing the activation of Nrf2/HO-1 signaling. The cytoprotective and antiapoptotic activities of SHM are abolished by the inhibition of HO-1 signaling. In further study, SHM restored the skin dryness and skin barrier disruption in UVB-exposed human keratinocytes. Based to these results, our study suggests that SHM protects the cells against UVB-induced cellular damages through the Nrf2/HO-1/NF-κB p65 signaling pathway and may be potentially useful for the prevention of UVB-induced skin damage.

scholarly journals MiR-664 Protects Against UVB Radiation-Induced HaCaT Cell Damage via Downregulating ARMC8

Dose-Response ◽  
2020 ◽  
Vol 18 (2) ◽  
pp. 155932582092923
Author(s):  
Chen Zhang ◽  
Xiongxiong Xie ◽  
Yawen Yuan ◽  
Yimeng Wang ◽  
Meijuan Zhou ◽  
...  
Keyword(s):  
Western Blot ◽  
Messenger Rna ◽  
Molecular Mechanisms ◽  
Cell Damage ◽  
Ultraviolet B ◽  
Cell Counting ◽  
Hacat Cells ◽  
Uvb Radiation ◽  
Related Factors ◽  
Radiation Induced

Background: MiR-664 has been demonstrated to play an important role in dermal diseases. However, the functions of miR-664 in ultraviolet B (UVB) radiation-induced keratinocytes damage remain to be elucidated. Objective: The present study aimed to investigate the molecular mechanisms under the UVB-induced keratinocytes damage and provide translational insights for future therapeutics and UVB protection. Methods: HaCaT cells were transfected with miR-664, either alone or combined with UVB irradiation. Levels of messenger RNA and protein were tested by quantitative real-time polymerase chain reaction and Western blot analyses. Cell proliferation, percentage of apoptotic cells, and expression levels of apoptosis-related factors were measured by Cell Counting Kit-8 assay, flow cytometry assay, and Western blot analysis, respectively. Results: We found that a significant increase in miR-664 was observed in UVB-induced HaCaT cells. Overexpressed miR-664 promoted cell vitalities and suppressed apoptosis of UVB-induced HaCaT cells. Additionally, the loss/gain of armadillo-repeat-containing protein 8 (ARMC8) rescued/blocked the effects of miR-664 on the proliferation of UVB-induced HaCaT cells. Conclusions: Our data demonstrate that miR-664 functions as a protective regulator in UVB-induced HaCaT cells via regulating ARMC8.

scholarly journals First person – Melisa Jovita Andrade

2021 ◽  
Vol 134 (12) ◽  
Keyword(s):  
Early Career ◽  
Ultraviolet B ◽  
Cellular Damage ◽  
First Person ◽  
Uvb Radiation ◽  
Skin Cells ◽  
Biomedical Innovation ◽  
University Of Technology ◽  
2D And 3D ◽  
Selection Of

ABSTRACT First Person is a series of interviews with the first authors of a selection of papers published in Journal of Cell Science, helping early-career researchers promote themselves alongside their papers. Melisa Jovita Andrade is first author on ‘RPA facilitates rescue of keratinocytes from UVB radiation damage through insulin-like growth factor-I signalling’, published in JCS. Melisa Jovita is a joint PhD student in the lab of Professor K. Satyamoorthy at Manipal School of Life Sciences, Manipal Academy of Higher Education, Manipal, Karnataka, India and Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Queensland, Australia, where her current research interests lie in understanding the cellular responses of skin cells to ultraviolet B radiation (UVBR) and the mechanistic pathways of cellular damage protection by growth factors in 2D and 3D photobiology human skin models.

scholarly journals Horse Oil Mitigates Oxidative Damage to Human HaCaT Keratinocytes Caused by Ultraviolet B Irradiation

2019 ◽  
Vol 20 (6) ◽  
pp. 1490
Author(s):  
Mei Piao ◽  
Kyoung Kang ◽  
Ao Zhen ◽  
Hee Kang ◽  
Young Koh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Matrix Metalloproteinase ◽  
Oxidative Damage ◽  
Reactive Oxygen ◽  
Ultraviolet B ◽  
Electromagnetic Spectrum ◽  
Oxygen Species ◽  
Uvb Radiation ◽  
Hacat Keratinocytes

Horse oil products have been used in skin care for a long time in traditional medicine, but the biological effects of horse oil on the skin remain unclear. This study was conducted to evaluate the protective effect of horse oil on ultraviolet B (UVB)-induced oxidative stress in human HaCaT keratinocytes. Horse oil significantly reduced UVB-induced intracellular reactive oxygen species and intracellular oxidative damage to lipids, proteins, and DNA. Horse oil absorbed light in the UVB range of the electromagnetic spectrum and suppressed the generation of cyclobutane pyrimidine dimers, a photoproduct of UVB irradiation. Western blotting showed that horse oil increased the UVB-induced Bcl-2/Bax ratio, inhibited mitochondria-mediated apoptosis and matrix metalloproteinase expression, and altered mitogen-activated protein kinase signaling-related proteins. These effects were conferred by increased phosphorylation of extracellular signal-regulated kinase 1/2 and decreased phosphorylation of p38 and c-Jun N-terminal kinase 1/2. Additionally, horse oil reduced UVB-induced binding of activator protein 1 to the matrix metalloproteinase-1 promoter site. These results indicate that horse oil protects human HaCaT keratinocytes from UVB-induced oxidative stress by absorbing UVB radiation and removing reactive oxygen species, thereby protecting cells from structural damage and preventing cell death and aging. In conclusion, horse oil is a potential skin protectant against skin damage involving oxidative stress.

scholarly journals Carbon Monoxide Partially Mediates Protective Effect of Resveratrol Against UVB-Induced Oxidative Stress in Human Keratinocytes

Antioxidants ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 432 ◽  
Author(s):  
Janice N. Averilla ◽  
Jisun Oh ◽  
Jong-Sang Kim
Keyword(s):  
Oxidative Stress ◽  
Carbon Monoxide ◽  
Radical Scavenging ◽  
Protoporphyrin Ix ◽  
Human Keratinocytes ◽  
Ultraviolet B ◽  
Related Factor ◽  
Uvb Radiation ◽  
Intracellular Ros ◽  
Tin Protoporphyrin

Based on the antioxidative effect of resveratrol (RES) in mitigating reactive oxygen species (ROS) production through the induction of nuclear factor-erythroid 2-related factor-2 (Nrf2)/heme oxigenase-1 (HO-1) signaling pathway, we investigated whether the protective activity of RES against ROS-mediated cytotoxicity is mediated by intracellular carbon monoxide (CO), a product of HO-1 activity, in ultraviolet B (UVB)-irradiated human keratinocyte HaCaT cells. The cells were exposed to UVB radiation following treatment with RES and/or CO-releasing molecule-2 (CORM-2). RES and/or CORM-2 upregulated HO-1 protein expression, accompanied by a gradual reduction of UVB-induced intracellular ROS levels. CORM-2 reduced intracellular ROS in the presence of tin protoporphyrin IX, an HO-1 inhibitor, indicating that the cytoprotection observed was mediated by intracellular CO and not by HO-1 itself. Moreover, CORM-2 decreased RES-stimulated mitochondrial quantity and respiration and increased the cytosolic protein expressions of radical-scavenging superoxide dismutases, SOD1 and SOD2. Taken together, our observations suggest that RES and intracellular CO act independently, at least partly, in attenuating cellular oxidative stress by promoting antioxidant enzyme expressions and inhibiting mitochondrial respiration in UVB-exposed keratinocytes.

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