scholarly journals Hydrogen-Generating Silica Material Prevents UVA-Ray-Induced Cellular Oxidative Stress, Cell Death, Collagen Loss and Melanogenesis in Human Cells and 3D Skin Equivalents

Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 76
Author(s):  
Li Xiao ◽  
Mai Mochizuki ◽  
Taka Nakahara ◽  
Nobuhiko Miwa
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Annexin V ◽  
Human Keratinocytes ◽  
Absorption Capacity ◽  
Human Cells ◽  
Skin Equivalents ◽  
Type Iv ◽  
Silica Material ◽  
3D Skin

Ultraviolet-A (UVA) irradiation induces harmful effects on skin cells and accelerates skin aging through oxidative stress. In this study, the effects of a hydrogen-generating silica material named ULH-002 against UVA injuries in human cells and 3D skin equivalents were investigated. The oxygen radical absorption capacity (ORAC) assay showed that both freshly prepared ULH-002 solutions and 7-day-old solutions exhibited equal peroxyl radical (ROO·) scavenging activities concentration-dependently. CellROX® green/orange staining showed that ULH-002 could reduce UVA-induced oxidative stress in human keratinocytes HaCaT and human gingival fibroblasts (HGFs). ULH-002 significantly prevented UVA-induced apoptotic/necrotic cell death and cell-viability decline in HGFs and keratinocytes, as shown by Annexin V/PI apoptosis assay and PrestoBlue assay, respectively. Immunostaining showed that ULH-002 prevented the UVA-induced deterioration of expression of both type IV and I collagens in the 3D skin equivalents, and similarly in monolayer HGFs. UVA-enhanced melanogenesis was observed in human melanocytes HMV-II and HMV-II cell-containing 3D skin equivalents, but markedly prevented by ULH-002 as demonstrated by Fontana–Masson’s staining. In conclusion, our data suggested that ULH-002 could protect human keratinocytes and fibroblasts from UVA-induced injuries, prevent the loss of type IV and I collagens, as well as reduce melanogenesis. ULH-002 might be developed as a skin care reagent in the cosmetic industry.

scholarly journals E-cigarette fluids and aerosol residues cause oxidative stress and an inflammatory response in human keratinocytes and 3D skin models

2021 ◽  
pp. 105234
Author(s):  
Careen Khachatoorian ◽  
Wentai Luo ◽  
Kevin J. McWhirter ◽  
James F. Pankow ◽  
Prue Talbot
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Human Keratinocytes ◽  
3D Skin

scholarly journals Black soybeans protect human keratinocytes from oxidative stress-induced cell death

2018 ◽  
Vol 6 (8) ◽  
pp. 2423-2430 ◽  
Author(s):  
Young Yoon ◽  
Yoon-Mi Lee ◽  
Sooji Song ◽  
Yu Young Lee ◽  
Kyung-Jin Yeum
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Human Keratinocytes

Selenium nanoparticles induce autophagy mediated cell death in human keratinocytes

Nanomedicine ◽  
2019 ◽  
Vol 14 (15) ◽  
pp. 1991-2010 ◽  
Author(s):  
Shrikant Kirwale ◽  
Venkatesh Pooladanda ◽  
Sowjanya Thatikonda ◽  
Sivasubramanian Murugappan ◽  
Amit Khurana ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Potential Role ◽  
Apoptotic Cell ◽  
Human Keratinocytes ◽  
Apoptotic Cell Death ◽  
Selenium Nanoparticles ◽  
Mitochondrial Membrane Depolarization ◽  
Need To Evaluate ◽  
Therapeutic Properties

Aim: Selenium nanoparticles (SeNPs) may have a potential role in treating dermal disorders due to its wide therapeutic properties, but there is a need to evaluate its toxicity in keratinocytes. The present study evaluated the molecular mechanism and mode of cell death induced by SeNPs on dermal keratinocytes. Materials & methods: SeNPs were synthesized, characterized and studied in human keratinocytes cells. Oxidative stress and mitochondrial membrane depolarization were evaluated by various techniques. Additionally, autophagy mediated apoptotic cell death was evaluated. Results: SeNPs induced oxidative stress and apoptotic cell death in keratinocytes by increasing autophagy through the formation of acidic lysosomes and autophagosomes. Conclusion: Overall, SeNPs induce the oxidative stress and autophagy mediated apoptotic cell death in human keratinocytes cells.

scholarly journals Phlorizin, an Active Ingredient ofEleutherococcus senticosus, Increases Proliferative Potential of Keratinocytes with Inhibition of MiR135b and Increased Expression of Type IV Collagen

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Hye-Ryung Choi ◽  
Kyung-Mi Nam ◽  
Hyun-Sun Lee ◽  
Seung-Hye Yang ◽  
Young-Soo Kim ◽  
...  
Keyword(s):  
Type Iv Collagen ◽  
Human Keratinocytes ◽  
Staining Intensity ◽  
Nuclear Antigen ◽  
Proliferative Potential ◽  
Main Ingredient ◽  
Skin Equivalents ◽  
Type Iv ◽  
Normal Human Keratinocytes ◽  
Normal Human

E. senticosusextract (ESE), known as antioxidant, has diverse pharmacologic effects. It is also used as an antiaging agent for the skin and phlorizin (PZ) is identified as a main ingredient. In this study, the effects of PZ on epidermal stem cells were investigated. Cultured normal human keratinocytes and skin equivalents are used to test whether PZ affects proliferative potential of keratinocytes and how it regulates these effects. Skin equivalents (SEs) were treated with ESE and the results showed that the epidermis became slightly thickened on addition of 0.002% ESE. The staining intensity of p63 as well as proliferating cell nuclear antigen (PCNA) is increased, and integrinα6 was upregulated. Analysis of ESE confirmed that PZ is the main ingredient. When SEs were treated with PZ, similar findings were observed. In particular, the expression of integrinα6, integrinβ1, and type IV collagen was increased. Levels of mRNA for type IV collagen were increased and levels of miR135b were downregulated. All these findings suggested that PZ can affect the proliferative potential of epidermal cells in part by microenvironment changes via miR135b downregulation and following increased expression of type IV collagen.

scholarly journals SPC212 Human Mesothelioma Cell Underwent Apoptosis, Oxidative Stress, Morhological Deformation Following Astaxanthin Treatment

2021 ◽  
Author(s):  
Sedat Kacar ◽  
Tuğba S. Sevimli ◽  
Varol Sahinturk
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Stress Test ◽  
Annexin V ◽  
Bioactive Compound ◽  
Cancer Types ◽  
Effective Doses ◽  
Annexin V Assay

Abstract Although astaxanthin (ASX) is one type of carotenoid, it is a more bioactive compound than other carotenoids. Despite its utilization against different cancer types, the effect of ASX on mesothelioma has yet to be well-studied. In this study, our goal is to ascertain how ASX will affect SPC212 human mesothelioma cells. First, the effective doses of ASX against SPC212 cells were uncovered by the MTT test. Thereafter, with flow cytometry analysis, Annexin-V and caspase 3/7 assay were implemented for the evaluation of apoptotic cell death and an oxidative stress test was carried out to determine how the free radicals changed. Ultimately, the cells’ morphology was examined under a light microscope. The effective doses of ASX were found as 50,100 and 200 µM. In Annexin V assay, the total apoptosis increased to around 12%, 30%, and %45 with increasing doses of ASX. In the caspase 3/7 assay, the total apoptosis was around %25 and %38 at 100 and 200 µM. In oxidative stress analysis, ROS-positive cells rose from 4.54 at the lowest dose to 86.95 at the highest dose. In morphological analysis, cellular shrinkage, decrease in cell density, swelling and vacuolations in some cells, membrane blebbing and apoptotic bodies are observed in ASX-treated cells. To conclude, the current study provided insights into the efficacy and effects of ASX against SPC212 mesothelioma cells regarding morphology, proliferation and cell death for future studies.

scholarly journals Oat (Avena sativa) Extract against Oxidative Stress-Induced Apoptosis in Human Keratinocytes

Molecules ◽  
2021 ◽  
Vol 26 (18) ◽  
pp. 5564
Author(s):  
Sooji Song ◽  
Yoon-Mi Lee ◽  
Yu Young Lee ◽  
Kyung-Jin Yeum
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Cell Death ◽  
Protective Effect ◽  
Avena Sativa ◽  
Ethanol Extract ◽  
Human Keratinocytes ◽  
Hacat Cells ◽  
Ethanol Extracts ◽  
Induced Apoptosis

Oat (Avena sativa) is well known for its various health benefits. The protective effect of oat extract against oxidative stress-induced apoptosis in human keratinocytes HaCaT was determined. First, extracts of two varieties of oat, Daeyang and Choyang, were analyzed for fat-soluble antioxidants such as α-tocotrienol, γ-oryzanols, lutein and zeaxanthin using an UPLC system and for antioxidant activity using a DPPH assay. Specifically, an 80% ethanol extract of Daeyang oat (Avena sativa cv. Daeyang), which had high amounts of antioxidants and potent radical scavenging activity, was further evaluated for protective effect against oxidative stress-induced cell death, intracellular reactive oxygen species levels, the phosphorylation of DNA damage mediating genes such as H2AX, checkpoint kinase 1 and 2, and p53 and the activation of apoptotic genes such as cleaved caspase-3 and 7 and poly (ADP-ribose) polymerase in HaCaT cells. The Daeyang and Choyang oat 80% ethanol extracts had 26.9 and 24.1 mg/100 g γ-oryzanols, 7.69 and 8.38 mg/100 g α-tocotrienol, 1.25 and 0.34 mg/100 g of lutein and 1.20 and 0.17 mg/100 g of zeaxanthin, respectively. The oat 80% ethanol extract treatment (Avena sativa cv. Daeyang) had a protective effect on oxidative stress-induced cell death in HaCaT cells. In addition, the oat 80% ethanol extracts led to a significant decrease in the intracellular ROS level at a concentration of 50–200 μg/mL, the attenuation of DNA damage mediating genes and the inhibition of apoptotic caspase activities in a dose dependent manner (50–200 μg/mL). Thus, the current study indicates that an oat (Avena sativa cv. Daeyang) extract rich in antioxidants, such as polyphenols, avenanthramides, γ-oryzanols, tocotrienols and carotenoids, has a protective role against oxidative stress-induced keratinocyte injuries and that oat may a useful source for oxidative stress-associated skin damage.

Reactive Oxygen Species Regulate Spontaneous and Fas-Mediated Apoptosis in SBDS-Deficient Cells.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 2036-2036
Author(s):  
Chhaya Ambekar ◽  
Bikul Das ◽  
Herman Yeger ◽  
Yigal Dror
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cell Growth ◽  
Cell Viability ◽  
Cell Survival ◽  
Annexin V ◽  
Necrotic Cell Death ◽  
Oxygen Species ◽  
Necrotic Cell

Abstract Background and hypotheses: Shwachman-Diamond syndrome (SDS) is an autosomal recessive disorder characterized by bone marrow failure, pancreatic insufficiency, and a marked propensity for myelodysplastic syndrome and leukemia. Approximately 90% of the patients have mutations in the SBDS gene, but the function of the gene is unknown. We previously showed that marrow cells from SDS patients and SBDS-deficient HeLa Cells are characterized by accelerated apoptosis, overexpression of Fas and hypersensitive to Fas stimulation. Involvement of reactive oxygen species (ROS; oxidative stress) have been shown to be related to Fas hypersensitivity and overexpression in a variety of cell types. Therefore, we hypothesized that functional deficiency in SBDS in cells that express Fas could lead to impaired ROS generation and a subsequent increase in spontaneous and Fas-mediated apoptosis and decrease in cell growth. Methods: We used shRNA-mediated SBDS-knockdown HeLa cells as a model. We investigated whether SBDS-deficiency increases ROS levels and if antioxidants can rescue the cell growth and apoptosis phenotype. To measure ROS formation cells were incubated with DCFH-DA and fluorescence measured in Gemini Spectra MAX microplate reader. Staining with annexin V and propidium iodide was done to determine apoptosis and necrotic cell death. MTT assay was used to measure cell viability. Results: ROS levels in SBDS knockdown cells were significantly increased compared to control. Apoptosis analysis by annexin V and propidium iodide showed a marked decrease in cell viability in the SBDS-knockdown cells. NAC treatment decreased ROS levels, enhanced ERK phosphorylation (pERK), improved cell viability, and decreased apoptotic and necrotic cell death. Stimulation of the Fas signaling pathway by CH-11 (activating anti-Fas antibody) and Fas ligand showed increased ROS production in SBDS Knockdown cells. CH-11 treatment showed a marked increase in apoptotic and necrotic cell death after 24 and 48hrs incubation. Cell viability decreased by 40% and 80% after 24 and 48hrs incubation with CH-11. Treatment with NAC lowered ROS levels, enhanced pERK expression, protected the cells from Fas-mediated early apoptosis and improved cell survival. Conclusion: We have demonstrated that stable loss of SBDS results in increased ROS levels, leading to apoptotic and necrotic cell death. Thus, increased baseline and Fas-stimulated ROS could result in increased sensitivity to apoptosis and necrotic cell death. NAC appeared to reverse the ROS-mediated decrease in cell survival and apoptotic cell death. Our data support the novel concept that SBDS may be a homeostatic regulator of oxidative stress

scholarly journals Relationship between Virus Replication and Apoptosis Events in IgM + Cells from Chicken Spleen and Bursa of Fabricius Infected with Malaysia Strain of Very Virulent Infectious Bursal Disease Virus

2018 ◽  
Vol 44 (1) ◽  
pp. 9 ◽  
Author(s):  
Kristeen Ye Wen Teo ◽  
Yeap Swee Keong ◽  
Tan Sheau Wei ◽  
Abdul Rahman Omar ◽  
Noorjahan Banu Alitheen
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Cell Death ◽  
Cell Viability ◽  
B Lymphocytes ◽  
Propidium Iodide ◽  
Annexin V ◽  
Bursa Of Fabricius ◽  
Chicken Spleen ◽  
Double Stain

Background: Infection of IBDV was reported to be endemic in worldwide including Malaysia and can be spread orally thru polluted fodder and water source, thus causing economic losses especially in commercial poultry industry. The infection resulted in depletion of B lymphocytes and subsequently destruction of the bursa which leaded to immunosuppression of the bird and it was postulated that the depletion of cells in the bursa was due to induction of apoptosis. In the current study, the infection of Malaysia isolated very virulent IBDV UPM0081 on IgM bearing B lymphocytes (IgM+ cells) from chicken spleen and bursa was compared.Materials, Methods & Results: A total of sixty eggs were obtained and raised until the age of 3 weeks old. The birds were divided into two groups (n = 30), which one of them served as control while IBDV strain UPM0081 was used to infect another group of birds at the concentration of 103 ELD50. The birds were observed and sacrificed at day 2, 4 and 5 post infections. Spleen and bursa of Fabricius were harvested and subjected to IgM+ cell enrichment using microbeads. The cell viability of enriched cells was assayed using MTT and cell cycle was analyzed using propidium iodide. Annexin V FITC and acridine orange/propidium iodide double stain assays were used to determine the event of apoptosis in the enriched IgM+ cells. Also, the IBDV viral load was also quantified by using real time PCR to evaluate the relationship between virus replication and apoptosis events in the infected chickens. Current results showed that the apoptotic events were observed to be significantly higher in IgM+ cells isolated from chicken bursa as compared to the cells isolated from spleen. The bursal B lymphocytes cell viability was observed to be decreasing following the infection of very virulent IBDV. The cells were then investigated of their apoptotic rate and data showed that increasing apoptotic cells (early and late apoptosis) were observed in AO/PI double stain as well as increment of SubG0/G1 population in the cell cycle analysis and also increment of Annexin V FITC bound cells in the apoptosis study. As for B lymphocytes from chicken spleen, the magnitude of damage caused by very virulent IBDV was not as severe as what being observed in the chicken bursa, with the cell viability drastically decreased on day 4 following IBDV infection.Discussion: IBDV caused severe destruction in bursa of Fabricius compared to spleen, in which cell death events in the former was reported to be directly caused by the virus. Apoptotic event in chicken spleen following IBDV infection was observed to be caused by oxidative stress. Thus, viral replication played a role in inducing bursal IgM+ cells death while such phenomenon was not observed in spleen isolated IgM+ cells. In summary, the cell death events of IgM+ cells in chicken spleen and bursa of Fabricius may be accounted by different factors upon infection with Malaysia strain of IBDV UPM0081. It is obvious that IgM+ cells from chicken bursa suffered from apoptotic cell death in an increasing manner considerably with time of infection and RNA load detected in the cells, which supported by previous literature that IBDV induces host cells apoptosis, with both VP2 and VP5 playing a role in binding and apoptosis. Meanwhile, the cell death events of B lymphocytes in chicken spleen was observed to be more relevant to other factors such as the oxidative stress or proinflammatory cytokines that caused by the virus infection rather than the viral RNA load.

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