scholarly journals Another Facet to the Anticancer Response to Lamellarin D: Induction of Cellular Senescence through Inhibition of Topoisomerase I and Intracellular Ros Production

Marine Drugs ◽  
2014 ◽  
Vol 12 (2) ◽  
pp. 779-798 ◽  
Author(s):  
Caroline Ballot ◽  
Alain Martoriati ◽  
Manel Jendoubi ◽  
Sébastien Buche ◽  
Pierre Formstecher ◽  
...  
Keyword(s):  
Cellular Senescence ◽  
Topoisomerase I ◽  
Ros Production ◽  
Intracellular Ros ◽  
Anticancer Response

scholarly journals FRI0370 DUAL OXIDASE MATURATION FACTOR 1 POSITIVELY REGULATES RANKL-INDUCED OSTEOCLASTOGENESIS VIA ACTIVATING REACTIVE OXYGEN SPECIES PRODUCTION AND TRAF6-MEDIATED SIGNALING

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 782.2-782
Author(s):  
C. H. Lee ◽  
C. H. Chung ◽  
Y. J. Choi ◽  
W. H. Yoo ◽  
J. Y. Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Osteoclast Differentiation ◽  
Reactive Oxygen ◽  
Mouse Bone Marrow ◽  
Ros Production ◽  
Oxygen Species ◽  
Maturation Factor ◽  
Intracellular Ros ◽  
Dual Oxidase ◽  
Rankl Stimulation

Background:Reactive oxygen species (ROS) are one of the significant factors of chemical or physical cell signaling in a wide variety of cell types including skeletal cells. Receptor activator of NF-βB ligand (RANKL) induces generation of intracellular ROS, which act as second messengers in RANKL-mediated osteoclastogenesis. Dual oxidase maturation factor 1 (Duoxa1) was first identified as aDrosophilaNumb-interacting protein (NIP), and has been associated with the maturation of ROS generating enzymes including dual oxidases (Duox1 and Duox2). In the progression of osteoclast differentiation using mouse bone marrow-derived macrophages (BMMs), we identified that only Duoxa1 level showed an effective change upon RANKL stimulation, but not Duox1, Duox2, and Duoxa2.Objectives:we hypothesized that Duoxa1 could independently act as a second messenger for RANKL stimulation and regulate ROS production during osteoclast differentiation.Methods:Using siRNA or retrovirus transduction and knockdown of Duoxa1 via siRNAResults:Duoxa1 level gradually increased during RANKL-induced osteoclast differentiation. We found that Duoxa1 regulated RANKL-stimulated osteoclast formation and bone resorption positively. knockdown of Duoxa1 via siRNA decreased the RANKL-induced ROS production. During Duoxa1-related control of osteoclastogenesis, activation of tumor necrosis factor receptor (TNFR)-associated factor 6 (TRAF6)-mediated early signaling molecules including MAPKs, Akt, IβB, Btk, and PLC 2 was affected, which sequentially modified the mRNA or protein expression levels of key transcription factors in osteoclastogenesis, such as c-Fos and NFATc1, as well as mRNA expression of osteoclast-specific markers including OSCAR, ATP6v0d2, and CtsK.Conclusion:Overall, our data indicate that Duoxa1 plays a crucial role in osteoclastogenesis via regulating RANKL-induced intracellular ROS production and activating TRAF6-mediated signaling.Disclosure of Interests:None declared

scholarly journals Vitamin E-Coated Dialyzer Inhibits Oxidative Stress

2017 ◽  
Vol 44 (4) ◽  
pp. 288-293 ◽  
Author(s):  
Shiho Yamadera ◽  
Yuya Nakamura ◽  
Masahiro Inagaki ◽  
Isao Ohsawa ◽  
Hiromichi Gotoh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Synthetic Polymer ◽  
Intracellular Reactive Oxygen Species ◽  
Ros Production ◽  
Oxygen Species ◽  
In Vitro Methods ◽  
Stress Effects ◽  
Intracellular Ros

Aim: To examine the effects of vitamin E-coated dialyzer on oxidative stress in vitro. Methods: A dialyzer with a synthetic polymer membrane (APS-11SA) and vitamin E-coated dialyzer (VPS-11SA) were connected to a blood tubing line, and U937 cells were circulated in the device. The circulating fluid was collected at 1, 2, 5, 10, 25, and 50 cycles, which are estimated numbers of passes through the dialyzer. Intracellular reactive oxygen species (ROS) production, malondialdehyde (MDA), and Cu/Zn-superoxide dismutase (SOD) were quantified. Results: Intracellular ROS production was increased in the first cycle by APS-11SA and was decreased throughout the experiment by VPS-11SA. Intracellular ROS production in the VPS-11SA device was lower, and MDA levels were decreased. MDA levels were lower during VPS-11SA processing than during APS-11SA processing. Cu/Zn-SOD levels remained unchanged. Conclusion: Our results highlight anti-oxidative-stress effects of a vitamin E-coated dialyzer.

8-Formylophiopogonanone B induces ROS-mediated apoptosis in nasopharyngeal carcinoma CNE-1 cells

2021 ◽  
Author(s):  
Ya-jing Zhang ◽  
Zhen-lin Mu ◽  
Ping Deng ◽  
Yi-dan Liang ◽  
Li-chuan Wu ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Cell Viability ◽  
Tumor Cells ◽  
High Efficiency ◽  
Pharmacological Action ◽  
Migration And Invasion ◽  
Ros Production ◽  
Biological Functions ◽  
Intracellular Ros

Abstract Cancer is one of the leading causes of death in the world. It is very important to find drugs with high efficiency, low toxicity, and low side effects for the treatment of cancer. Flavonoids and their derivatives with broad biological functions have been recognized as anti-tumor chemicals. 8-Formylophiopogonanone B (8-FOB), a naturally existed homoisoflavonoids with rarely known biological functions, needs pharmacological evaluation. In order to explore the possible anti-tumor action of 8-FOB, we used six types of tumor cells to evaluate in vitro effects of this agent on cell viability and tested the effects on clone formation ability, scratching wound-healing, and apoptosis. In an attempt to elucidate the mechanism of pharmacological action, we examined 8-FOB-induced intracellular oxidative stress and -disrupted mitochondrial function. Results suggested that 8-FOB could suppress tumor cell viability, inhibit cell migration and invasion, induce apoptosis, and elicit intracellular ROS production. Among these six types of tumor cells, the nasopharyngeal carcinoma CNE-1 cells were the most sensitive cancer cells to 8-FOB treatment. Intracellular ROS production played a pivotal role in the anti-tumor action of 8-FOB. Our present study is the first to document that 8-FOB has anti-tumor activity in vitro and increases intracellular ROS production, which might be responsible for its anti-tumor action. The anti-tumor pharmacological effect of 8-FOB is worthy of further investigation.

Protective effect of nigella sativa extract and thymoquinone on serum/glucose deprivation-induced PC12 cells death

2011 ◽  
Vol 26 (S2) ◽  
pp. 908-908
Author(s):  
H.R. Sadeghnia ◽  
S.H. Mousavi ◽  
Z. Tayarani-Najaran ◽  
M. Asghari
Keyword(s):  
Cell Viability ◽  
Pc12 Cells ◽  
Neurodegenerative Disorders ◽  
Nigella Sativa ◽  
Glucose Deprivation ◽  
Serum Glucose ◽  
Ros Production ◽  
Protective Effects ◽  
Intracellular Ros

The serum/glucose deprivation (SGD)-induced cell death in cultured PC12 cells represents a useful in vitro model for the study of brain ischemia and neurodegenerative disorders.Nigella sativa L. and its active component, thymoquinone (TQ) have been known as a source of antioxidants. In the present study, the protective effects of N. sativa and TQ on cell viability and reactive oxygen species (ROS) production in cultured PC12 cells were investigated under SGD conditions. PC12 Cells were pretreated with different concentrations of N. sativa extract (15.62–250 μg/ml) and TQ (1.17–150 μM) for 2 h and then subjected to SGD for 6 or 18 h. Cell viability was quantitated by MTT assay. Intracellular ROS production was measured by flow cytometry using 2’,7’-dichlorofluorescin diacetate (DCF-DA) as a probe. SGD induced significant cells toxicity after 6, 18, or 24 h (p < 0.001). Pretreatment with N. sativa (15.62–250 μg/ml) and TQ (1.17–37.5 μM) reduced SGD-induced cytotoxicity in PC12 cells after 6 and 18 h. A significant increase in intracellular ROS production was seen following SGD (p < 0.001). N. sativa (250 μg/ml, p < 0.01) and TQ (2.34, 4.68, 9.37 μM, p < 0.01) pretreatment reversed the increased ROS production following ischemic insult. The experimental results suggest that N. sativa extract and TQ protects the PC12 cells against SGD-induced cytotoxicity via antioxidant mechanisms. Our findings might raise the possibility of potential therapeutic application of N. sativa extract and TQ for managing cerebral ischemic and neurodegenerative disorders.

scholarly journals Oxidative Stress in Cell Death and Cardiovascular Diseases

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Tao Xu ◽  
Wei Ding ◽  
Xiaoyu Ji ◽  
Xiang Ao ◽  
Ying Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Cardiovascular Diseases ◽  
Death Process ◽  
Ros Production ◽  
Disease Treatment ◽  
Physiological Conditions ◽  
Intracellular Ros ◽  
Cell Death Process ◽  
Molecular Components ◽  
Multiple Signaling

ROS functions as a second messenger and modulates multiple signaling pathways under the physiological conditions. However, excessive intracellular ROS causes damage to the molecular components of the cell, which promotes the pathogenesis of various human diseases. Cardiovascular diseases are serious threats to human health with extremely high rates of morbidity and mortality. Dysregulation of cell death promotes the pathogenesis of cardiovascular diseases and is the clinical target during the disease treatment. Numerous studies show that ROS production is closely linked to the cell death process and promotes the occurrence and development of the cardiovascular diseases. In this review, we summarize the regulation of intracellular ROS, the roles of ROS played in the development of cardiovascular diseases, and the programmed cell death induced by intracellular ROS. We also focus on anti-ROS system and the potential application of anti-ROS strategy in the treatment of cardiovascular diseases.

scholarly journals Carbon Black Nanoparticles Promote Endothelial Activation and Lipid Accumulation in Macrophages Independently of Intracellular ROS Production

PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e106711 ◽  
Author(s):  
Yi Cao ◽  
Martin Roursgaard ◽  
Pernille Høgh Danielsen ◽  
Peter Møller ◽  
Steffen Loft
Keyword(s):  
Carbon Black ◽  
Lipid Accumulation ◽  
Endothelial Activation ◽  
Ros Production ◽  
Carbon Black Nanoparticles ◽  
Intracellular Ros

Synthesis of 4-aryl-1,2,3-triazolyl appended natural coumarin-related compounds with antiproliferative and radical scavenging activities and intracellular ROS production modification

2017 ◽  
Vol 41 (15) ◽  
pp. 7531-7543 ◽  
Author(s):  
A. Bistrović ◽  
N. Stipaničev ◽  
T. Opačak-Bernardi ◽  
M. Jukić ◽  
S. Martinez ◽  
...  
Keyword(s):  
Antiproliferative Activity ◽  
Radical Scavenging Activity ◽  
Radical Scavenging ◽  
K562 Cells ◽  
Ros Production ◽  
Scavenging Activity ◽  
Intracellular Ros ◽  
Natural Coumarin ◽  
Related Compounds

Diverse natural coumarin-based compounds linked to aryl via a 1,2,3-triazole spacer with antiproliferative activity against K562 cells, radical scavenging activity and a decrease of ROS production were provided.

scholarly journals oxLDL-mediated cellular senescence is associated with increased NADPH oxidase p47phox recruitment to caveolae

2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Jing Wang ◽  
Yuzhi Bai ◽  
Xia Zhao ◽  
Jing Ru ◽  
Ning Kang ◽  
...  
Keyword(s):  
Cellular Senescence ◽  
Clinical Intervention ◽  
Ros Generation ◽  
Ros Production ◽  
Caveolin 1 ◽  
Cellular Ageing ◽  
Vascular Endothelia ◽  
Membrane Target ◽  
High Degree ◽  
Atherosclerotic Changes

Atherosclerosis develops as a consequence of inflammation and cell senescence. In critical factors involved in the atherosclerotic changes, reactive oxygen species (ROS) generation is considered a leading cause. While NADPH oxidases, particularly NOX2, are the main sources of ROS, how they are regulated in the disease is incompletely understood. In addition, how caveolae, the membrane structure implicated in oxLDL deposition under vascular endothelia, is involved in the oxLDL-mediated ROS production remains mostly elusive. We report here that macrophages exposed to oxLDL up-regulate its caveolin-1 expression, and the latter in turn up-regulates NOX2 p47phox level. This combination effect results in increased cellular senescence. Interestingly, oxLDL treatment causes the p47phox residing in the cytosol to translocate to the caveolae. Immunoprecipitation assays confirms that cavelin-1 is in high degree association with p47phox. These results suggest caveolin-1 may serve as the membrane target for p47phox and as a switch for ROS production following oxLDL exposure. Our results reveal a previously unknown molecular event in oxLDL-mediated cellular ageing, and may provide a target for clinical intervention for atherosclerosis.

Acetate Suppresses Lipopolysaccharide-stimulated Nitric Oxide Production in Primary Rat Microglia but not in BV-2 Microglia Cells

2020 ◽  
Vol 14 (2) ◽  
pp. 253-260
Author(s):  
Mitsuaki Moriyama ◽  
Yasunori Nishimura ◽  
Ryosuke Kurebayashi ◽  
Tomoki Minamihata ◽  
Kenji Kawabe ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Ethics Committees ◽  
No Production ◽  
Dependent Manner ◽  
Intraventricular Administration ◽  
Ros Production ◽  
Primary Microglia ◽  
Inhibitory Effects ◽  
Intracellular Ros ◽  
Dose Dependent

Aims: To show that acetate attenuates neuroinflammatory responses in activated microglia. Background: Dietary acetate supplementation alleviates neuroglial activation in a rat model of neuroinflammation induced by intraventricular administration of lipopolysaccharide (LPS). However, the precise mechanism(s) underlying the anti-inflammatory effect of acetate is not fully understood. Objective: To determine whether acetate has inhibitory effects on LPS-induced neuroinflammatory responses in microglia. Methods: We examined LPS-stimulated nitric oxide (NO) production in primary rat microglia and BV-2 cells. Protein expression of inducible NO synthase (iNOS) was determined by western blot analysis. The intracellular generation of reactive oxygen species (ROS) and glutathione (GSH) were also evaluated. Results: In primary microglia, acetate decreased LPS-stimulated NO production in a dose-dependent manner, reaching significance at greater than 10 mM, and cell viability was not affected. Acetate suppressed LPS-induced expression of iNOS protein concomitantly with the decrease in NO. The LPS-induced increase in intracellular ROS production was attenuated by acetate. In addition, acetate prevented LPSinduced reduction of GSH. Notably, such suppressive effects of acetate on NO and ROS production were not observed in BV-2 cells. Conclusion: These findings suggest that acetate may alleviate neuroinflammatory responses by attenuating NO and ROS production in primary microglia but not in BV-2 cells. Other: All animals received humane care and the animal protocols used in this study were approved by the Ethics Committees for Animal Experimentation.

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