scholarly journals Echinacoside Alleviates UVB Irradiation-Mediated Skin Damage via Inhibition of Oxidative Stress, DNA Damage, and Apoptosis

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Di Zhang ◽  
Chengtao Lu ◽  
Zhe Yu ◽  
Xiayin Wang ◽  
Li Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Histopathological Examination ◽  
Ultraviolet B ◽  
Ros Generation ◽  
Antioxidant Enzyme Activities ◽  
Skin Damage ◽  
Uvb Irradiation ◽  
Uvb Exposure

Ultraviolet B (UVB) irradiation has been known to cause skin damage, which is associated with oxidative stress, DNA damage, and apoptosis. Echinacoside is a phenylethanoid glycoside isolated from Herba Cistanches, which exhibits strong antioxidant activity. In this study, we evaluate the photoprotective effect of echinacoside on UVB-induced skin damage and explore the potential molecular mechanism. BALB/c mice and HaCaT cells were treated with echinacoside before UVB exposure. Histopathological examination was used to evaluate the skin damage. Cell viability, lactate dehydrogenase (LDH) levels, antioxidant enzyme activities, reactive oxygen species (ROS) generation, DNA damage, and apoptosis were measured as well. Western blot was used to measure the expression of related proteins. The results revealed that pretreatment of echinacoside ameliorated the skin injury; attenuated oxidative stress, DNA damage, and apoptosis caused by UVB exposure; and normalized the protein levels of ATR, p53, PIAS3, hnRNP K, PARP, and XPA. To summarize, echinacoside is beneficial in the prevention of UVB-induced DNA damage and apoptosis of the skin in vivo and in vitro.

Photoprotection of maqui berry against ultraviolet B-induced photodamage in vitro and in vivo

2020 ◽  
Vol 11 (3) ◽  
pp. 2749-2762 ◽  
Author(s):  
Ling Chen ◽  
Gao Zhou ◽  
Xiao-Shan Meng ◽  
Hui-Ying Fu ◽  
Qi-Gui Mo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Ultraviolet B ◽  
Uvb Irradiation ◽  
Maqui Berry ◽  
Berry Extracts ◽  
Cellular Dna

Maqui berry extracts could ameliorate oxidative stress, cellular DNA damage, and inflammation induced by UVB-irradiation in vitro and in vivo.

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.

scholarly journals Allicin Protects PC12 Cells Against 6-OHDA-Induced Oxidative Stress and Mitochondrial Dysfunction via Regulating Mitochondrial Dynamics

2015 ◽  
Vol 36 (3) ◽  
pp. 966-979 ◽  
Author(s):  
Hao Liu ◽  
Ping Mao ◽  
Jia Wang ◽  
Tuo Wang ◽  
Chang-Hou Xie
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Pc12 Cells ◽  
Atp Synthesis ◽  
Ros Generation ◽  
Antioxidant Enzyme Activities ◽  
Protective Effects ◽  
Cytochrome C Release ◽  
Endogenous Antioxidant

Background: Parkinson disease (PD) is a common adult-onset neurodegenerative disorder, and PD related neuronal injury is associated with oxidative stress and mitochondrial dysfunction. Allicin, the main biologically active compound derived from garlic, has been shown to exert various anti-oxidative and anti-apoptotic activities in in vitro and in vivo studies. Methods: The present study aimed to investigate the potential protective role of allicin in an in vitro PD model induced by 6-hydroxydopamine (6-OHDA) in PC12 cells. The protective effects were measured by cell viability, decreased lactate dehydrogenase (LDH) release and flow cytometry, and the anti-oxidative activity was determined by reactive oxygen species (ROS) generation, lipid peroxidation and the endogenous antioxidant enzyme activities. Mitochondrial function in PC12 cells was detected by mitochondrial membrane potential (MMP) collapse, cytochrome c release, mitochondrial ATP synthesis, and the mitochondrial Ca2+ buffering capacity. To investigate the potential mechanism, we also measured the expression of mitochondrial biogenesis factors, mitochondrial morphological dynamic changes, as well as detected mitochondrial dynamic proteins by western blot. Results: We found that allicin treatment significant increased cell viability, and decreased LDH release and apoptotic cell death after 6-OHDA exposure. Allicin also inhibited ROS generation, reduced lipid peroxidation and preserved the endogenous antioxidant enzyme activities. These protective effects were associated with suppressed mitochondrial dysfunction, as evidenced by decreased MMP collapse and cytochrome c release, preserved mitochondrial ATP synthesis, and the promotion of mitochondrial Ca2+ buffering capacity. In addition, allicin significantly enhanced mitochondrial biogenesis and prevented fragmentation of mitochondrial network after 6-OHDA treatment. The results of western blot analysis showed that the 6-OHDA induced decrease in the expression of optic atrophy type 1 (Opa-1), increase in mitochondrial fission 1 (Fis-1) and dynamin-related protein 1 (Drp-1) were all partially revised by allicin. Conclusion: In summary, our data strongly suggested that allicin treatment can exert protective effects against PD related neuronal injury through inhibiting oxidative stress and mitochondrial dysfunction with dynamic changes.

scholarly journals Keratinocyte Growth Factor 2 Ameliorates UVB-Induced Skin Damage via Activating the AhR/Nrf2 Signaling Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Shuang Gao ◽  
Keke Guo ◽  
Yu Chen ◽  
Jungang Zhao ◽  
Rongrong Jing ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Growth Factor ◽  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
Keratinocyte Growth Factor ◽  
Ros Production ◽  
Skin Damage ◽  
Nrf2 Signaling Pathway ◽  
Uvb Exposure

Objective: Exposure to ultraviolet B (UVB) can cause skin damage through oxidative stress, DNA damage, and apoptosis. Keratinocyte growth factor (KGF) has been shown to reduce the content of intracellular reactive oxygen species (ROS) following UVB exposure, a role that is crucial for the efficient photoprotection of skin. The present study evaluated the photoprotective effect of KGF-2 on UVB-induced skin damage and explored its potential molecular mechanism.Methods: To evaluate the effect of KGF-2 on UVB-induced damage ex vivo, a human epidermal full-thickness skin equivalent was pretreated without or with KGF-2 and then exposed to UVB and the levels of histopathological changes, DNA damage, inflammation, and apoptosis were then evaluated. The ability of KGF-2 to protect the cells against UVB-inflicted damage and its effect on ROS production, apoptosis, and mitochondrial dysfunction were determined in HaCaT cells.Results: Pretreatment of the epidermis with KGF-2 ameliorated the extent of photodamage. At the cellular level, KGF-2 could attenuate ROS production, apoptosis, DNA damage, and mitochondrial dysfunction caused by UVB exposure. KGF-2 could also activate the aryl hydrocarbon receptor (AhR) to trigger the Nrf2 signaling pathway.Conclusion: Taken together, our findings suggested that KGF-2 could ameliorate UVB-induced skin damage through inhibiting apoptosis, reducing oxidative stress, and preventing DNA damage and mitochondrial dysfunction via regulating AhR/Nrf2 signaling pathway.

scholarly journals Standardized Edible Bird's Nest Extract Prevents UVB Irradiation-Mediated Oxidative Stress and Photoaging in the Skin

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1452
Author(s):  
Ok-Kyung Kim ◽  
Dakyung Kim ◽  
Minhee Lee ◽  
Seong-Hoo Park ◽  
Wakana Yamada ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ultraviolet B ◽  
Type I ◽  
Ceramide Synthase ◽  
Hairless Mice ◽  
In Vivo Models ◽  
Uvb Irradiation ◽  
Edible Bird’S Nest

We investigated whether standardized edible bird’s nest extract (BNE-PK) can prevent ultraviolet B (UVB) irradiation-mediated oxidative stress and photoaging in the skin using in vitro and in vivo models. BNE-PK increased skin hydration by hyaluronic acid synthesis and activation of ceramide synthase in UVB-irradiated hairless mice and HaCaT cells. Furthermore, BNE-PK suppressed melanogenesis by down-regulation of the cAMP/PKA/CREB/MITF/TRP-1/TRP-2/tyrosinase pathway in UVB-irradiated hairless mice and 3-isobutyl-1-methylxanthine (IBMX)-treated B16F10 cells. In UVB-irradiated hairless mice, BNE-PK attenuated the wrinkle formation-related JNK/c-FOS/c-Jun/MMP pathway and activated the TGF-βRI/SMAD3/pro-collagen type I pathway during UVB-mediated oxidative stress. Based on these findings, our data suggest that BNE-PK may potentially be used for the development of effective natural anti-photoaging functional foods for skin health.

scholarly journals Tryptophan Photoproduct FICZ Upregulates IL1A, IL1B, and IL6 Expression via Oxidative Stress in Keratinocytes

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yuka Tanaka ◽  
Hiroshi Uchi ◽  
Akiko Hashimoto-Hachiya ◽  
Masutaka Furue
Keyword(s):  
Proinflammatory Cytokine ◽  
Protein Product ◽  
Ultraviolet B ◽  
Ros Generation ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Hacat Keratinocytes ◽  
Uvb Irradiation ◽  
Aryl Hydrocarbon ◽  
Uvb Exposure

Ultraviolet B (UVB) irradiation activates the aryl hydrocarbon receptor (AHR), generates the reactive oxygen species (ROS), and induces the production of proinflammatory cytokines such as IL1A, IL1B, and IL6. 6-Formylindolo[3,2-b]carbazole (FICZ) is a tryptophan-derived photoproduct that is induced by UVB irradiation and activates the AHR. However, its role in upregulating proinflammatory cytokine expression has never been investigated. Here, we demonstrated that FICZ enhanced ROS generation in human HaCaT keratinocytes in an AHR-dependent manner. FICZ also upregulated the expression of IL1A and IL1B, as well as the expression of IL6 and the production of its protein product, in an AHR- and ROS-dependent fashion. Here, we demonstrate that the actions of FICZ can substitute for the hazardous effects of UVB exposure, contributing to the further understandings of the mechanisms which UVB harms organisms.

Hypothyroidism induces oxidative stress and DNA damage in breast

2021 ◽  
Author(s):  
Milena Simões Peixoto ◽  
Andressa de Vasconcelos e Souza ◽  
Iris Soares Andrade ◽  
Carolina de Carvalho el Giusbi ◽  
Caroline Coelho Faria ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Dna Damage ◽  
Genomic Instability ◽  
Redox Balance ◽  
Ros Generation ◽  
Antioxidant Enzyme Activities ◽  
Oxidative Stress Biomarkers ◽  
Stress Biomarkers ◽  
Mcf10a Cells

Breast cancer and thyroid dysfunctions have been associated for decades. Although many studies suggest a biological correlation, the mechanisms linking these two pathologies have not been elucidated. Reactive oxygen species (ROS) can oxidize lipids, proteins, and DNA molecules and may promote tumor initiation. Hence, we aimed at evaluating the mammary redox balance and genomic instability in a model of experimental hypothyroidism. Female Wistar rats were treated with 0.03% methimazole for 7 or 21 days to evaluate ROS generation, antioxidant enzyme activities, and oxidative stress biomarkers, as well as genomic instability. After 7 days, lower catalase, GPx, and DUOX activities were detected in the breast of hypothyroid group compared to the control while the levels of 4-hydroxynonenal (HNE) were higher. In addition, hypothyroid group showed an increase in γH2Ax/H2Ax ratio. 21-days hypothyroid group had increased catalase and SOD activities, without significant differences between groups in the levels of oxidative stress biomarkers and DNA damage. TSH-treated MCF10A cells showed a higher extracellular, intracellular, and mitochondrial ROS production. Additionally, greater DNA damage was observed in these cells, demonstrated by a higher comet tail DNA percentage and increased 53BP1 foci. Finally, we found that TSH treatment was not able to alter cell viability. The Genome Cancer Atlas (TGCA) data showed that high TSHR expression is associated with more invasive breast cancer types. In conclusion, we demonstrate that oxidative stress and DNA damage in breast are early events of experimental hypothyroidism. Moreover, high TSH levels induce oxidative stress and genomic instability in mammary cells.

Protocatechuic Acid Protects Platelets from Apoptosis via Inhibiting Oxidative Stress-Mediated PI3K/Akt/GSK3β Signaling

2021 ◽  
Author(s):  
Fuli Ya ◽  
Kongyao Li ◽  
Hong Chen ◽  
Zezhong Tian ◽  
Die Fan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Protocatechuic Acid ◽  
Human Platelets ◽  
Ros Generation ◽  
Inhibitory Effects ◽  
Platelet Apoptosis ◽  
Phosphatidylserine Exposure ◽  
Underlying Mechanisms

AbstractOxidative stress plays crucial roles in initiating platelet apoptosis that facilitates the progression of cardiovascular diseases (CVDs). Protocatechuic acid (PCA), a major metabolite of anthocyanin cyanidin-3-O-β-glucoside (Cy-3-g), exerts cardioprotective effects. However, underlying mechanisms responsible for such effects remain unclear. Here, we investigate the effect of PCA on platelet apoptosis and the underlying mechanisms in vitro. Isolated human platelets were treated with hydrogen peroxide (H2O2) to induce apoptosis with or without pretreatment with PCA. We found that PCA dose-dependently inhibited H2O2-induced platelet apoptosis by decreasing the dissipation of mitochondrial membrane potential, activation of caspase-9 and caspase-3, and decreasing phosphatidylserine exposure. Additionally, the distributions of Bax, Bcl-xL, and cytochrome c mediated by H2O2 in the mitochondria and the cytosol were also modulated by PCA treatment. Moreover, the inhibitory effects of PCA on platelet caspase-3 cleavage and phosphatidylserine exposure were mainly mediated by downregulating PI3K/Akt/GSK3β signaling. Furthermore, PCA dose-dependently decreased reactive oxygen species (ROS) generation and the intracellular Ca2+ concentration in platelets in response to H2O2. N-Acetyl cysteine (NAC), a ROS scavenger, markedly abolished H2O2-stimulated PI3K/Akt/GSK3β signaling, caspase-3 activation, and phosphatidylserine exposure. The combination of NAC and PCA did not show significant additive inhibitory effects on PI3K/Akt/GSK3β signaling and platelet apoptosis. Thus, our results suggest that PCA protects platelets from oxidative stress-induced apoptosis through downregulating ROS-mediated PI3K/Akt/GSK3β signaling, which may be responsible for cardioprotective roles of PCA in CVDs.

Acrylamide-induced oxidative stress in human erythrocytes

2009 ◽  
Vol 28 (10) ◽  
pp. 611-617 ◽  
Author(s):  
Betul Catalgol ◽  
Gül Özhan ◽  
Buket Alpertunga
Keyword(s):  
Oxidative Stress ◽  
Reduced Glutathione ◽  
Human Erythrocytes ◽  
Antioxidant Enzyme Activities ◽  
Total Glutathione ◽  
Sod Activity ◽  
Spectrophotometric Methods ◽  
Low Concentrations ◽  
Different Doses

Acrylamide (AA), a widely used industrial chemical, is shown to be neurotoxic, mutagenic and carcinogenic. This study was carried out to investigate the effects of different doses of AA on lipid peroxidation (LPO), haemolysis, methaemoglobin (MetHb) and antioxidant system in human erythrocytes in vitro. Erythrocyte solutions were incubated with 0.10, 0.25, 0.50 and 1.00 mM of AA at 37°C for 1 hour. At the end of the incubation, malondialdehyde (MDA), an end product of LPO, was determined by liquid chromatography (LC) while total glutathione, reduced glutathione (GSH) levels, activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzymes and the rates of haemolysis and MetHb were determined by spectrophotometric methods. All of the studied concentrations of AA increased MetHb formation and SOD activity, and induced MDA formation and haemolysis due to the destruction of erythrocyte cell membrane. AA caused a decrease in the activities of GSH-Px, CAT and GSH levels. However, these effects of AA were seen only at higher concentrations than AA intake estimated for populations in many countries. We suggest that LPO process may not be involved in the toxic effects of AA in low concentrations, although the present results showed that the studied concentrations of AA exert deteriorating effects on antioxidant enzyme activities, LPO process and haemolysis.

8. Evaluation of Snow Fungus Polysaccharides on benzo[a]pyrene-induced DNA Damage

2018 ◽  
Author(s):  
Daisy Liu
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Free Radical ◽  
Radical Scavenging ◽  
Chinese Hamster ◽  
Negative Control ◽  
Lung Fibroblasts ◽  
Protective Effects ◽  
Tremella Fuciformis

Snow fungus, Tremella fuciformis, has been demonstrated to have numerous health benefits including purported chemopreventive properties due to free radical-scavenging ability. Protective effects derived from snow fungus polysaccharides are evaluated on Chinese hamster lung fibroblasts (CCL-39) exposed to carcinogen benzo[a]pyrene known to cause free radical formation and oxidative stress to cells. In this experiment, it was hypothesized that the naturally occurring polysaccharides in snow fungus are able to protect against or reduce oxidative stress-induced DNA damage. Polysaccharides were isolated through an alkaline extraction and in-vitro digestion. DNA damage was measured using the single-cell gel electrophoresis comet assay after exposure to benzo[a]pyrene and polysaccharide extract to lung fibroblasts. Results were calculated using the mean and standard deviation data of tail length and area, respectively. Each damaged cell was measured and analyzed through ImageJ Editing Software. The results indicate a promising trend which depict snow fungus polysaccharides yielding lower levels of DNA damage compared to cells exposed to benzo[a]pyrene and compared to the negative control (phosphate buffered saline and Dulbecco’s cell medium). This study suggests polysaccharides from Tremella fuciformis could truly prevent cellular DNA damage by protecting against oxidative stress.

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