Nickel Oxide (NiO) Nanoparticles Induce Loss of Cell Viability in Yeast Mediated by Oxidative Stress

2018 ◽  
Vol 31 (8) ◽  
pp. 658-665 ◽  
Author(s):  
Cátia A. Sousa ◽  
Helena M. V. M. Soares ◽  
Eduardo V. Soares
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Nickel Oxide ◽  
Nio Nanoparticles

Exploring the characteristics of the nickel oxide nanoparticles via Sol - gel method

2020 ◽  
Vol 3 (3) ◽  
Author(s):  
Jothi M ◽  
Sowmiya K
Keyword(s):  
Nickel Oxide ◽  
Ph Value ◽  
Lattice Structure ◽  
Sol Gel ◽  
Systematic Change ◽  
Average Crystalline Size ◽  
Nio Nanoparticles ◽  
Nickel Oxide Nanoparticles ◽  
X Ray ◽  
Vis Spectroscopy

Nickel Oxide (NiO) is an important transition metal oxide with cubic lattice structure. NiO is thermally stable that is suitable for tremendous applications in the field of optic, ceramic,glass, electro-chromic coatings, plastics, textiles, nanowires, nanofibers, electronics,energy technology, bio-medicine, magnetism and so on. In this present study, NiO nanoparticles were successfully synthesized by sol-gel technique. Nano-sols were prepared by dissolving Nickel-Chloride [NiCl2.6H2O] in NaOH solvent and were converted into nano structured gel on precipitation. A systematic change in preparation parameters like calcination temperature, time, pH value has been noticed in order to predict the influence on crystallite size. Then the prepared samples were characterized by the X-ray Diffraction Spectroscopic (XRD), UV-VIS Spectroscopy, Fourier Transform Infra-Red Spectroscopy (FTIR), Energy Dispersive X-ray Spectroscopy (EDX), Scanning Electron Microscopy (SEM) and Particle Size Analyzer (PSA). From XRD, the average crystalline-size has been calculated by Debye-Scherrer Equation and it was found to be 12.17 nm and the band gap energy of Nickel oxide (NiO) from UV studies reveals around 3.85 eV. Further, EDX and FTIR studies, confirm the presences of NiO nanoparticles. The SEM study exhibits the spherical like morphology of Nickel oxide (NiO). Further from PSA, the mean value of NiO nanoparticles has been determined.

MiR-485-5p Promotes Neuron Survival through Mediating Rac1/Notch2 Signaling Pathway after Cerebral Ischemia/Reperfusion

2020 ◽  
Vol 17 (3) ◽  
pp. 259-266 ◽  
Author(s):  
Xuan Chen ◽  
Sumei Zhang ◽  
Peipei Shi ◽  
Yangli Su ◽  
Dong Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Therapeutic Option ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Small Gtpase ◽  
Luciferase Reporter ◽  
Pathological Feature ◽  
In Cells

Objective: Ischemia-reperfusion (I/R) injury is a pathological feature of ischemic stroke. This study investigated the regulatory role of miR-485-5p in I/R injury. Methods: SH-SY5Y cells were induced with oxygen and glucose deprivation/reoxygenation (OGD/R) to mimic I/R injury in vitro. Cells were transfected with designated constructs (miR-485- 5p mimics, miR-485-5p inhibitor, lentiviral vectors overexpressing Rac1 or their corresponding controls). Cell viability was evaluated using the MTT assay. The concentrations of lactate dehydrogenase, malondialdehyde, and reactive oxygen species were detected to indicate the degree of oxidative stress. Flow cytometry and caspase-3 activity assay were used for apoptosis assessment. Dual-luciferase reporter assay was performed to confirm that Rac family small GTPase 1 (Rac1) was a downstream gene of miR-485-5p. Results: OGD/R resulted in decreased cell viability, elevated oxidative stress, increased apoptosis, and downregulated miR-485-5p expression in SH-SY5Y cells. MiR-485-5p upregulation alleviated I/R injury, evidenced by improved cell viability, decreased oxidative markers, and reduced apoptotic rate. OGD/R increased the levels of Rac1 and neurogenic locus notch homolog protein 2 (Notch2) signaling-related proteins in cells with normal miR-485-5p expression, whereas miR- 485-5p overexpression successfully suppressed OGD/R-induced upregulation of these proteins. Furthermore, the delivery of vectors overexpressing Rac1 in miR-485-5p mimics-transfected cells reversed the protective effect of miR-485-5p in cells with OGD/R-induced injury. Conclusion: This study showed that miR-485-5p protected cells following I/R injury via targeting Rac1/Notch2 signaling suggest that targeted upregulation of miR-485-5p might be a promising therapeutic option for the protection against I/R injury.

Hydrogen peroxide and quercetin induced changes on cell viability, apoptosis and oxidative stress in HepG2 cells

2020 ◽  
Vol 01 ◽  
Author(s):  
Ayşe Mine Yılmaz ◽  
Gökhan Biçim ◽  
Kübra Toprak ◽  
Betül Karademir Yılmaz ◽  
Irina Milisav ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Hydrogen Peroxide ◽  
Cell Viability ◽  
Hepg2 Cells ◽  
Proteasome Activity ◽  
Cell Cycle Phases ◽  
Induced Changes ◽  
And Oxidative Stress ◽  
Quercetin Treatment

Background: Different cellular responses influence the progress of cancer. In this study, we have investigated the effect of hydrogen peroxide and quercetin induced changes on cell viability, apoptosis and oxidative stress in human hepatocellular carcinoma (HepG2) cells. Methods: The effects of hydrogen peroxide and quercetin on cell viability, cell cycle phases and oxidative stress related cellular changes were investigated. Cell viability was assessed by WST-1 assay. Apoptosis rate, cell cycle phase changes and oxidative stress were measured by flow cytometry. Protein expressions of p21, p27, p53, NF-Kβ-p50 and proteasome activity were determined by Western blot and fluorometry, respectively. Results: Hydrogen peroxide and quercetin treatment resulted in decreased cell viability and increased apoptosis in HepG2 cells. Proteasome activity was increased by hydrogen peroxide but decreased by quercetin treatment. Conclusion: Both agents resulted in decreased p53 protein expression and increased cell death by different mechanisms regarding proteostasis and cell cycle phases.

scholarly journals Phytosynthetic Fabrication of Lanthanum Ion-Doped Nickel Oxide Nanoparticles Using Sesbania grandiflora Leaf Extract and Their Anti-Microbial Properties

Crystals ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 124
Author(s):  
Srihasam Saiganesh ◽  
Thyagarajan Krishnan ◽  
Golla Narasimha ◽  
Hesham S. Almoallim ◽  
Sulaiman Ali Alhari ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Optical Properties ◽  
Rare Earth ◽  
Nickel Oxide ◽  
Photoelectron Spectroscopy ◽  
Metal Oxide Nanoparticles ◽  
Oxide Nanoparticles ◽  
Nio Nanoparticles ◽  
X Ray ◽  
Sesbania Grandiflora

Over the past few years, the photogenic fabrication of metal oxide nanoparticles has attracted considerable attention, owing to the simple, eco-friendly, and non-toxic procedure. Herein, we fabricated NiO nanoparticles and altered their optical properties by doping with a rare earth element (lanthanum) using Sesbania grandiflora broth for antibacterial applications. The doping of lanthanum with NiO was systematically studied. The optical properties of the prepared nanomaterials were investigated through UV-Vis diffuse reflectance spectra (UV-DRS) analysis, and their structures were studied using X-ray diffraction analysis. The morphological features of the prepared nanomaterials were examined by scanning electron microscopy and transmission electron microscopy, their elemental structure was analyzed by energy-dispersive X-ray spectral analysis, and their oxidation states were analyzed by X-ray photoelectron spectroscopy. Furthermore, the antibacterial action of NiO and La-doped NiO nanoparticles was studied by the zone of inhibition method for Gram-negative and Gram-positive bacterial strains such as Escherichia coli and Bacillus sublitis. It was evident from the obtained results that the optimized compound NiOLa-04 performed better than the other prepared compounds. To the best of our knowledge, this is the first report on the phytosynthetic fabrication of rare-earth ion Lanthanum (La3+)-doped Nickel Oxide (NiO) nanoparticles and their anti-microbial studies.

scholarly journals Cytotoxicity induced by new spiral mesoporous silica nanorods via specific surface area and ROS accumulation in HeLa cells

2020 ◽  
Vol 1 (9) ◽  
pp. 3556-3564
Author(s):  
Lan She ◽  
Miao Sun ◽  
Xinfang Li ◽  
Anfeng Kang ◽  
Feng Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mesoporous Silica ◽  
Cell Viability ◽  
Specific Surface ◽  
Surface Area ◽  
Specific Surface Area ◽  
Hela Cells ◽  
Ros Accumulation ◽  
Silica Nanorods

Results indicated that the effect of MSNRs on cell viability and cellular oxidative stress was related to specific surface area.

scholarly journals Beneficial effect of 1,25 dihydroxyvitamin D3 on cytokine-treated human pancreatic islets

2001 ◽  
Vol 169 (1) ◽  
pp. 161-168 ◽  
Author(s):  
R Riachy ◽  
B Vandewalle ◽  
S Belaich ◽  
J Kerr-Conte ◽  
V Gmyr ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Cell Viability ◽  
Pancreatic Islets ◽  
Mhc Class I ◽  
Class I ◽  
Insulin Content ◽  
Hsp70 Expression ◽  
Human Pancreatic Islets ◽  
Mnsod Activity

We examined whether 1,25 dihydroxyvitamin D(3) (1,25 D(3)), the active form of vitamin D involved in the regulation of the immune system, may also protect human pancreatic islet cells from destruction induced by cytokines. In this study, we specifically investigated the effect of 1,25 D(3) on oxidative stress and major histocompatibility complex (MHC) induction, both implicated in cytokine-induced islet cell dysfunction and destruction. We also investigated the effects of 1,25 D(3) on interleukin (IL)-6, a pleiotropic cytokine implicated in the pathogenesis of immunoinflammatory disorders. Human pancreatic islets, isolated from heart-beating donors, were treated with a combination of three cytokines, IL-1beta+tumor necrosis factor alpha+interferon gamma, in the presence or absence of vitamin D, and compared with with untreated control cells. Metabolic activity was assessed by cell viability and insulin content. Oxidative stress was estimated by heat shock protein 70 (hsp70) expression, cell manganese superoxide dismutase (MnSOD) activity and nitrite release, a reflexion of nitric oxide (NO) synthesis. Variation of immunogenicity of islet preparations was determined by analysis of the MHC class I and class II transcripts. Inflammatory status was evaluated by IL-6 production. After 48 h of contact with cytokines, insulin content was significantly decreased by 40% but cell viability was not altered. MHC expression significantly increased six- to sevenfold as well as NO and IL-6 release (two- to threefold enhancement). MnSOD activity was not significantly induced and hsp70 expression was not affected by the combination of cytokines. The addition of 1,25 D(3) significantly reduced nitrite release, IL-6 production and MHC class I expression which then became not significantly different from controls. These results suggest that the effect of 1,25 D(3) in human pancreatic islets cells may be a reduction of the vulnerability of cells to cytotoxic T lymphocytes and a reduction of cytotoxic challenge. Hence, 1,25 D(3) might play a role in the prevention of type 1 diabetes and islet allograft rejection.

Toxicity of Cerium Oxide Nanoparticles in Human Lung Cancer Cells

2006 ◽  
Vol 25 (6) ◽  
pp. 451-457 ◽  
Author(s):  
Weisheng Lin ◽  
Yue-wern Huang ◽  
Xiao-Dong Zhou ◽  
Yinfa Ma
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Lactate Dehydrogenase ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cerium Oxide ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Human Lung Cancer Cells

With the fast development of nanotechnology, the nanomaterials start to cause people’s attention for potential toxic effect. In this paper, the cytotoxicity and oxidative stress caused by 20-nm cerium oxide (CeO2) nanoparticles in cultured human lung cancer cells was investigated. The sulforhodamine B method was employed to assess cell viability after exposure to 3.5, 10.5, and 23.3 μg/ml of CeO2 nanoparticles for 24, 48, and 72 h. Cell viability decreased significantly as a function of nanoparticle dose and exposure time. Indicators of oxidative stress and cytotoxicity, including total reactive oxygen species, glutathione, malondialdehyde, α-tocopherol, and lactate dehydrogenase, were quantitatively assessed. It is concluded from the results that free radicals generated by exposure to 3.5 to 23.3 μg/ml CeO2 nanoparticles produce significant oxidative stress in the cells, as reflected by reduced glutathione and α-tocopherol levels; the toxic effects of CeO2 nanoparticles are dose dependent and time dependent; elevated oxidative stress increases the production of malondialdehyde and lactate dehydrogenase, which are indicators of lipid peroxidation and cell membrane damage, respectively.

Matrine Protects PC12 Cells Against Aβ25–35-Induced Cytotoxicity, Oxidative Stress, Inflammation, Neuronal Apoptosis and Cell Senescence

2021 ◽  
Vol 11 (9) ◽  
pp. 1691-1697
Author(s):  
Huanli Zhang ◽  
Zhen Zhang
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Pc12 Cells ◽  
Neuronal Apoptosis ◽  
Inflammatory Responses ◽  
Neuronal Damage ◽  
Cell Senescence ◽  
Tunel Staining ◽  
Elisa Assay ◽  
Amyloid A

Background and Objectives: Beta-amyloid (Aβ) has pivotal functions in the pathogenesis of Alzheimer’s Disease (AD). The main purpose of this study is to explore the protective role and possible mechanisms of matrine against Aβ25–35-induced neurotoxicity in PC12 cells. Materials and Methods: A vitro model that involved Aβ25–35-induced neuronal damage in PC12 cells was adopted in the present study. Cell viability and apoptosis of PC12 cells were determined by CCK-8 assay and TUNEL staining, respectively. Intracellular ROS levels were determined by DCFH-DA probe and levels of TNFα, IL-6 and IL-1β were assessed by ELISA assay. In addition, telomerase reverse transcriptase (TERT) levels were determined by ELISA assay and telomere lengths were examined by real-time quantitative PCR analysis to assess telomerase activities. Furthermore, vital proteins related to cell apoptosis and hallmarks of senescence were detected by western blot analysis. Results: Matrine (10, 20, 50 μg/ml) dose-dependently protected cell viability against Aβ25–35 cytotoxicity in PC12 cells. Meanwhile, matrine at 10, 20, 50 μg/ml markedly reduced ROS production and downregulated the levels of TNFα, IL-6 and IL-1β in Aβ25–35-injuried PC12 cells. The results also proved that matrine may restore telomerase activities and telomere lengths in Aβ25–35-injuried PC12 cells by inhibiting inflammatory responses and oxidative stress. Neuronal apoptosis induced by Aβ25–35 were reversed upon cotreatment with matrine. Moreover, matrine markedly mitigated Aβ25–35 induced cell senescence in a concentration-dependentmanner. Conclusion: Our findings demonstrated that matrine protected PC12 cells against Aβ25–35-induced cytotoxicity, oxidative stress, inflammation, neuronal apoptosis and cell senescence.

Silibinin-Albumin Nanoparticles: Characterization and Biological Evaluation Against Oxidative Stress-Stimulated Neurotoxicity Associated with Alzheimer’s Disease

2021 ◽  
Vol 17 (6) ◽  
pp. 1123-1130
Author(s):  
Qichen Pan ◽  
Yunchao Ban ◽  
Lijun Xu
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Antioxidant Activity ◽  
Cell Viability ◽  
Antioxidant Activities ◽  
Drug Loading ◽  
Biological Evaluation ◽  
Neural Cells ◽  
Nanoparticles Characterization

Alzheimer’s disease (AD) is strongly associated with oxidative stress which can damage neural cells. Silibinin has shown potential antioxidative effects. However, due to its low solubility in water, silibinin provides low biological activity and bioavailability. Therefore, to increase its pharmacological effects, silibilin was encapsulated into human serum albumin (HSA) nanoparticles and well-characterized by DLS and TEM techniques. The antioxidant activity of silibinin-HSA nanoparticles was evaluated on LPS-induced oxidative stress in neuron-like cells (SH-SY5Y) through MTT, antioxidant activity and apoptotic assay. It was shown that the mean diameter of HSA and silibinin-HSA nanoparticles were 88 and 105 nm, respectively with a drug loading of 24.08%, drug encapsulation rate of 94.72%, and the yield of silibinin-HSA nanoparticles of around 83.41% and the HSA nano-formulation released silibinin for 15 h. The results displayed that cell viability was reduced by LPS (10 μg/mL), who’s also determined to stimulate oxidative stress and apoptosis. However, co-incubation of cells with silibinin (50 μg/mL) or silibinin-HSA nanoparticles led to the recovery of cell viability, activation of SOD and CAT, increase of GSH content, and reduction of ROS level, Caspase-3 activity and fragmentation of DNA. It was also indicated that the neuroprotective and antioxidant activities of silibinin-HAS nanoparticles was greater than free silibinin, indicating that using albumin can be a potential formulation approach for improving the antioxidant efficacy of silibinin.

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