scholarly journals Protective Effect of Spirulina-Derived C-Phycocyanin against Ultraviolet B-Induced Damage in HaCaT Cells

Medicina ◽  
2021 ◽  
Vol 57 (3) ◽  
pp. 273
Author(s):  
Young Ah Jang ◽  
Bo Ae Kim
Keyword(s):  
Antioxidant Defense System ◽  
Skin Aging ◽  
Ultraviolet B ◽  
Control Group ◽  
Hacat Cells ◽  
Uvb Radiation ◽  
Skin Damage ◽  
Blue Green Algae ◽  
Radiation Group ◽  
Skin Wrinkles

Background and objectives: Reactive oxygen species (ROS) overwhelm the antioxidant defense system, induce oxidative stress, and increase matrix metalloproteinase (MMP) expression, resulting in skin aging. Thus, preventing ultraviolet B (UVB)-induced skin damage can attenuate skin aging. Spirulina (a biomass of cyanobacteria, also called blue-green algae) is comprised of prokaryotes, whereas microalgae are eukaryotes and are rich in phycocyanin, a powerful antioxidant. Materials and Methods: Here, we investigated the photoprotective effects of spirulina-derived C-phycocyanin (C-PC) against UVB radiation using keratinocytes (HaCaT cells). Results: UVB radiation increased MMP-1 and MMP-9 expression but decreased involucrin, filaggrin, and loricrin expression. C-PC showed no toxicity at concentrations of 5–80 μg/mL in terms of HaCaT cell viability. UVB-irradiated HaCaT cells had a 50.8% survival rate, which increased to 80.3% with C-PC treatment. MMP expression increased with UVB treatment, whereas MMP-1 and MMP-9 concentrations decreased with C-PC treatment. UVB reduced involucrin, filaggrin, and loricrin expression in HaCaT cells, but 80 μg/mL C-PC increased their expression by >25%. In the UVB radiation group, dichlorofluorescin diacetate fluorescence intensity in HaCaT cells increased by 81.6% compared with that in the control group, whereas ROS production was reduced by 51.2% and 55.1% upon treatment with 40 and 80 μg/mL C-PC, respectively. Conclusions: C-PC might reduce or prevent skin aging by reducing UVB irradiation-induced skin wrinkles and free radicals.

scholarly journals Laminarin Attenuates Ultraviolet-Induced Skin Damage by Reducing Superoxide Anion Levels and Increasing Endogenous Antioxidants in the Dorsal Skin of Mice

Marine Drugs ◽  
2020 ◽  
Vol 18 (7) ◽  
pp. 345 ◽  
Author(s):  
Ji Hyeon Ahn ◽  
Dae Won Kim ◽  
Cheol Woo Park ◽  
Bora Kim ◽  
Hyejin Sim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Anion ◽  
Collagen Fibers ◽  
Ultraviolet B ◽  
Control Group ◽  
Dorsal Skin ◽  
Skin Damage ◽  
Superoxide Anion Production ◽  
Uvb Exposure ◽  
Immunohistochemical Studies

A number of studies have demonstrated that marine carbohydrates display anti-oxidant, anti-melanogenic, and anti-aging activities in the skin. Laminarin (LA), a low-molecular-weight polysaccharide, is found in brown algae. The benefits of LA in ultraviolet B (UVB) induced photodamage of the skin have not been reported. The aim of this study was to investigate the effects of pre-treated LA on histopathological changes and oxidative damage in mouse dorsal skin on day 5, following repeated UVB exposure. Histopathology, Western blot analysis and immunohistochemical studies showed that epidermal thickness in the UVB group was significantly increased; however, the thickness in the UVB group treated with LA (LA/UVB group) was less compared with that of the UVB group. Collagen fibers in the dermis of the UVB group were significantly decreased and destroyed, whereas, in the LA/UVB group, the density of collagen fibers was significantly increased compared with that of the UVB group. Oxidative stress due to superoxide anion production measured via dihydroethidium fluorescence staining was dramatically increased in the UVB group, whereas in the LA/UVB group, the oxidative stress was significantly decreased. Expressions of SOD1, glutathione peroxidase and catalase were markedly reduced in the UVB group, whereas in the LA/UVB group, they were significantly higher along with SOD2 than in the control group. Taken together, our results indicate that LA pretreatment prevents or attenuates skin damage, by decreasing oxidative stress and increasing antioxidant enzymes in mouse dorsal skin.

Repeated exposures of human skin equivalent to low doses of ultraviolet-B radiation lead to changes in cellular functions and accumulation of cyclobutane pyrimidine dimers

2001 ◽  
Vol 79 (4) ◽  
pp. 507-515 ◽  
Author(s):  
Nadine Chouinard ◽  
Jean-Philippe Therrien ◽  
David L Mitchell ◽  
Marielle Robert ◽  
Régen Drouin ◽  
...  
Keyword(s):  
Dna Damage ◽  
Repeated Exposure ◽  
Ultraviolet B ◽  
Skin Equivalent ◽  
Basal Cells ◽  
Uvb Radiation ◽  
Skin Damage ◽  
Cyclobutane Pyrimidine Dimers ◽  
Biochemical Alterations ◽  
Pyrimidine Dimers

Chronic exposure to sunlight may induce skin damage such as photoaging and photocarcinogenesis. These harmful effects are mostly caused by ultraviolet-B (UVB) rays. Yet, less is known about the contribution of low UVB doses to skin damage. The aim of this study was to determine the tissue changes induced by repeated exposure to a suberythemal dose of UVB radiation. Human keratinocytes in monolayer cultures and in skin equivalent were irradiated daily with 8 mJ/cm2 of UVB. Then structural, ultrastructural, and biochemical alterations were evaluated. The results show that exposure to UVB led to a generalized destabilization of the epidermis structure. In irradiated skin equivalents, keratinocytes displayed differentiated morphology and a reduced capacity to proliferate. Ultrastructural analysis revealed, not only unusual aggregation of intermediate filaments, but also disorganized desmosomes and larger mitochondria in basal cells. UVB irradiation also induced the secretion of metalloproteinase-9, which may be responsible for degradation of type IV collagen at the basement membrane. DNA damage analysis showed that both single and repeated exposure to UVB led to formation of (6–4) photoproducts and cyclobutane pyrimidine dimers. Although the (6–4) photoproducts were repaired within 24 h after irradiation, cyclobutane pyrimidine dimers accumulated over the course of the experiment. These studies demonstrate that, even at a suberythemal dose, repeated exposure to UVB causes significant functional and molecular damage to keratinocytes, which might eventually predispose to skin cancer.Key words: UVB, keratinocytes, skin structure, DNA damage, photoproducts.

scholarly journals UVB irradiation of human platelet concentrates does not prevent HLA alloimmunization in recipients

Blood ◽  
1994 ◽  
Vol 84 (10) ◽  
pp. 3524-3531
Author(s):  
MA Grijzenhout ◽  
MI Aarts-Riemens ◽  
FR de Gruijl ◽  
H van Weelden ◽  
HC van Prooijen
Keyword(s):  
Cell Death ◽  
Hla Antigens ◽  
Ultraviolet B ◽  
Control Group ◽  
Unexpected Finding ◽  
Uvb Radiation ◽  
Platelet Concentrates ◽  
Uvb Irradiation ◽  
Hla Class I Antigens ◽  
Delayed Cell Death

Exposure of platelet concentrates (PCs) to ultraviolet B radiation (UVB) has been advocated as an alternative method for prevention of the onset of HLA sensitization in recipients. In this study, pooled PCs were irradiated in a Haemonetics UV irradiator (Haemonetics Corp, Braintree, MA) at a dose that did not induce platelet activation. The effect of UVB irradiation on prevention of primary HLA sensitization was evaluated in a prospective controlled clinical study performed in cardiac patients undergoing cardiopulmonary bypass. Patients were treated with filtered red blood cells and a single transfusion of either standard (control group) or UVB-irradiated (UVB group) pooled platelets prepared from 12 donors. Five of 39 patients in the control group and 6 of 62 patients in the UVB group developed allo-antibodies against HLA antigens, which is not significantly different (P = .62). This unexpected finding prompted us to check the efficacy of UVB irradiation. We determined UVB-specific DNA damage in cells by measuring the fluorescence from a labeled specific monoclonal antibody against thymine dimers. With this novel flow cytometer technique, we estimated in UVB-irradiated leukocytes in saline that a mean fluorescence intensity (MFI) of 47 +/- 2 arbitrary units (n = 6) correlated with abolition of alloreactivity in mixed lymphocyte cultures and delayed cell death (within 72 hours). MFI in leukocytes suspended in plasma and exposed to the clinical dose of UVB was sixfold higher (310 +/- 41 arbitrary units) and resulted in early cell death (within 24 hours). We hypothesize that this high level of UVB radiation induces fragmentation of the leukocytes. As a consequence, the poor results of UVB irradiation may be explained by the onset of HLA- alloimmunization induced by soluble donor HLA class I antigens processed and presented by host antigen-presenting cells.

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 Mirabilis Jalapa L. Protein as Inductor of Apoptosis on UVB-induced Skin Damage in Mice

2017 ◽  
Vol 16 (3) ◽  
pp. 423-427
Author(s):  
Atina Hussaana ◽  
Sismindari ◽  
Sitarina Widyarini ◽  
Sudjadi ◽  
Zullies Ikawati
Keyword(s):  
Protective Effect ◽  
Dna Fragmentation ◽  
Caspase 3 ◽  
Control Group ◽  
Peak Time ◽  
Uvb Radiation ◽  
Skin Damage ◽  
Uvb Irradiation ◽  
L Protein ◽  
Mirabilis Jalapa

Background: Mirabilis jalapa L. protein (MJ-Protein) has been shown to have antioxidant and anti-inflammatory effects in vitro. Thus, it has a potential protective effect against ultraviolet B (UVB)-induced skin damage.Objective: To determine the protective effect and mechanism of MJ protein in UVB-radiation exposed mouse skin.Methods: In this experimentalstudy, 30 female BALB/c mice aged 6 weeks were exposed to a single dose of UVB irradiation with 3 minimal erythema doses (MEDs) and continued with the treatment of 0.6 mg MJ-Protein topically. The number of apoptotic body (sunburn cells) formed in epidermal layers of mouse dorsal skin was assessed at 1, 24, 48, 72, 96 and 120h after UVB irradiation was compared to that of the control group. The difference in the sunburn cells number between two groups were analyzed using independent T-test with the level of significance of 0.05. The apoptosis mechanism was confirmed qualitatively by caspase-3 and DNA fragmentation analysis in vitro.Results:At 24 h after the UVB exposure (peak time for sunburn cells formation), there was a significant increase in the sunburn cells number in the group treated with topical application of MJ-Protein. There was increased caspase-3 expression and DNA fragmentation in HeLa cells treated with MJ-Protein.Conclusions: MJ-Protein protects againts UVB-induced skin damage in mice trough apoptosis induction.Bangladesh Journal of Medical Science Vol.16(3) 2017 p.423-427

scholarly journals The Metabolite Profile in Culture Supernatant of Aster yomena Callus and Its Anti-Photoaging Effect in Skin Cells Exposed to UVB

Plants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 659
Author(s):  
Woo Sik Kim ◽  
Jeong Hun Seo ◽  
Jae-In Lee ◽  
Eun-Sil Ko ◽  
Sang-Min Cho ◽  
...  
Keyword(s):  
Culture Supernatant ◽  
Transforming Growth Factor ◽  
Skin Diseases ◽  
Scale Up ◽  
Ultraviolet B ◽  
Related Factor ◽  
Type I ◽  
Nuclear Factor ◽  
Hacat Cells ◽  
Skin Damage

Aster yomena (A. yomena) extract has anti-inflammatory, antioxidant, anti-asthma, and anti-atopic effects. However, the commercial use of A. yomena extract requires a long processing time with specific processing steps (including heat treatment and ethanol precipitation), and there are various environmental problems. We aimed to build a system to produce A. yomena extract by culturing the callus in a bioreactor that can allow rapid process scale-up to test the effect of extract (AYC-CS-E) isolated from culture supernatant of A. yomena callus on photoaging of human keratinocytes (HaCaT) caused by ultraviolet B (UVB) exposure. Through screening analysis based on ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC/Q-TOF-MS), 17 major metabolites were tentatively identified from AYC-CS-E for the first time. The suppression of cell proliferation caused by UVB was effectively alleviated in UVB-irradiated HaCaT cells treated with AYC-CS-E. Treatment with AYC-CS-E strongly induced the formation of type I procollagen and the inhibition of elastase in UVB-irradiated HaCaT cells and significantly reduced the expression of matrix metalloproteinase (MMP)-1. In addition, treatment of UVB-irradiated HaCaT cells with AYC-CS-E effectively improved various factors associated with an inflammatory reaction, skin damage recovery, skin moisture retention, and hyper-keratinization caused by photoaging, such as reactive oxygen species (ROS), pro-inflammatory cytokines, transforming growth factor beta (TGF-β), MMP-3, MMP-9, filaggrin, hyaluronic acid synthase 2 (HAS-2), keratin 1 (KRT-1), nuclear factor-kappa B (NF-κB), and nuclear factor erythroid 2-related factor 2 (Nrf2) at the gene and protein levels. These results suggest that AYC-CS-E can be used as a cosmetic ingredient for various skin diseases caused by photoaging, and the current callus culture system can be used commercially to supply cosmetic ingredients.

scholarly journals Almond Consumption Increased UVB Resistance in Healthy Asian Women

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 319-319
Author(s):  
Susanne Henning ◽  
Jason Li ◽  
Gail Thames ◽  
Omar Bari ◽  
Patrick Tran ◽  
...  
Keyword(s):  
Skin Aging ◽  
Ultraviolet B ◽  
In Vivo Studies ◽  
Asian Women ◽  
Skin Extract ◽  
Uvb Radiation ◽  
Facial Skin ◽  
Uvb Exposure

Abstract Objectives Almonds are a rich source of phenolic and polyphenolic compounds, which have antioxidant activity. In vitro and in vivo studies have demonstrated that topical application of almond oil and almond skin extract reduces UVB-induced photoaging. Ultraviolet-B (UVB) protection by oral almond consumption has not been previously studied in humans. It was the objective to investigate whether oral almond consumption can increase resistance to UVB radiation and reduce skin aging in healthy Asian women. Methods Thirty-nine female participants (18–45 years) with Fitzpatrick skin type II-IV were randomly assigned to consume either 1.5 oz of almonds or 1.8 oz of pretzels daily for 12 weeks. Minimal erythema dose (MED) was determined using a standardized protocol, which determined the minimal radiation inducing erythema on the inner arm 24 hours following UVB exposure. Facial skin texture was evaluated by two dermatologists using the Clinician's Erythema Assessment scale and Allergan Roughness scale. Facial melanin index, hydration, sebum, and erythema were determined using a cutometer. Results Women who consumed almonds, experienced a significant increase in MED from 415 ± 64 to 487 ± 59 (18.7 ± 19.2%, P = 0.006) from baseline to week 12 compared to women in the pretzel group from 415 ± 67 to 421 ± 67 (1.8 ± 11.1%). The exposure time to reach minimal erythema was also increased significantly in the almond group from 160 ± 23 to 187 ± 25 (17.5 ± 22.2%) compared to the pretzel group from 165 ± 27 to 166 ± 25 (1.7 ± 14%) (p=0.026). There were no differences noted between the groups consuming almonds versus pretzels in Allergan roughness, melanin, hydration, or sebum on facial skin. Conclusions Our findings suggest that daily oral almond consumption may lead to enhanced protection from UVB photodamage by increasing the MED. Protection from other UV radiation was not tested and therefore almond consumption will not replace other methods of sun protection such as application of sunscreen or wearing protective closing. Funding Sources Almond Board of California.

scholarly journals Protective effect of total flavonoids from boxthorn leaf against UVB irradiation-induced skin injury

2021 ◽  
Vol 18 (9) ◽  
pp. 1943-1947
Author(s):  
Qing Yu ◽  
Ying Shen ◽  
Yadan Gan ◽  
Liang Zheng
Keyword(s):  
Protective Effect ◽  
Negative Control Group ◽  
Negative Control ◽  
Ultraviolet B ◽  
Control Group ◽  
Total Flavonoids ◽  
Skin Damage ◽  
Skin Injury ◽  
Uvb Irradiation ◽  
Base Group

Purpose: To investigate the protective effect of total flavonoids from boxthorn leaf against skin injury induced by UVB irradiation, and to elucidate the underlying mechanism of action. Method: Healthy female mice (n = 100) were randomly divided into four groups: normal control group, UV negative control group, cream base group, and boxthorn leaf total flavonoid (BLTF) group, with 25 mice in each group. The mice in each group were irradiated with ultraviolet B (UVB) irradiation instrument for 1.5 h daily for 3 weeks. Mice in the cream base group were smeared with cream base on their backs, while mice in BLTF group were smeared with 15 mg/g boxthorn BLTF cream. The control and negative control group mice were not treated. Changes in superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) levels were determined using standard methods. Results: Compared to the negative control group, the levels of SOD and GSH-Px in the control group and BLTF were significantly elevated, while MDA levels declined significantly (p < 0.05). Although higher GSH-Px and SOD levels, and lower MDA were seen in the cream base group than in negative control group, these indices were comparable for the two groups (p > 0.05). Conclusion: The total flavonoids of boxthorn leaves improve resistance to UVB-induced skin damage by regulating SOD, MDA and GSH-Px levels in the skin of mice. Thus, they exert protective effects on the skin.

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 irradiation of human platelet concentrates does not prevent HLA alloimmunization in recipients

Blood ◽  
1994 ◽  
Vol 84 (10) ◽  
pp. 3524-3531 ◽  
Author(s):  
MA Grijzenhout ◽  
MI Aarts-Riemens ◽  
FR de Gruijl ◽  
H van Weelden ◽  
HC van Prooijen
Keyword(s):  
Cell Death ◽  
Hla Antigens ◽  
Ultraviolet B ◽  
Control Group ◽  
Unexpected Finding ◽  
Uvb Radiation ◽  
Platelet Concentrates ◽  
Uvb Irradiation ◽  
Hla Class I Antigens ◽  
Delayed Cell Death

Abstract Exposure of platelet concentrates (PCs) to ultraviolet B radiation (UVB) has been advocated as an alternative method for prevention of the onset of HLA sensitization in recipients. In this study, pooled PCs were irradiated in a Haemonetics UV irradiator (Haemonetics Corp, Braintree, MA) at a dose that did not induce platelet activation. The effect of UVB irradiation on prevention of primary HLA sensitization was evaluated in a prospective controlled clinical study performed in cardiac patients undergoing cardiopulmonary bypass. Patients were treated with filtered red blood cells and a single transfusion of either standard (control group) or UVB-irradiated (UVB group) pooled platelets prepared from 12 donors. Five of 39 patients in the control group and 6 of 62 patients in the UVB group developed allo-antibodies against HLA antigens, which is not significantly different (P = .62). This unexpected finding prompted us to check the efficacy of UVB irradiation. We determined UVB-specific DNA damage in cells by measuring the fluorescence from a labeled specific monoclonal antibody against thymine dimers. With this novel flow cytometer technique, we estimated in UVB-irradiated leukocytes in saline that a mean fluorescence intensity (MFI) of 47 +/- 2 arbitrary units (n = 6) correlated with abolition of alloreactivity in mixed lymphocyte cultures and delayed cell death (within 72 hours). MFI in leukocytes suspended in plasma and exposed to the clinical dose of UVB was sixfold higher (310 +/- 41 arbitrary units) and resulted in early cell death (within 24 hours). We hypothesize that this high level of UVB radiation induces fragmentation of the leukocytes. As a consequence, the poor results of UVB irradiation may be explained by the onset of HLA- alloimmunization induced by soluble donor HLA class I antigens processed and presented by host antigen-presenting cells.

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