scholarly journals The H2S Donor GYY4137 Stimulates Reactive Oxygen Species Generation in BV2 Cells While Suppressing the Secretion of TNF and Nitric Oxide

Molecules ◽  
2018 ◽  
Vol 23 (11) ◽  
pp. 2966 ◽  
Author(s):  
Milica Lazarević ◽  
Emanuela Mazzon ◽  
Miljana Momčilović ◽  
Maria Basile ◽  
Giuseppe Colletti ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Microglial Cells ◽  
Oxygen Species ◽  
Bv2 Cells ◽  
The Central Nervous System

GYY4137 is a hydrogen sulfide (H2S) donor that has been shown to act in an anti-inflammatory manner in vitro and in vivo. Microglial cells are among the major players in immunoinflammatory, degenerative, and neoplastic disorders of the central nervous system, including multiple sclerosis, Parkinson’s disease, Alzheimer’s disease, and glioblastoma multiforme. So far, the effects of GYY4137 on microglial cells have not been thoroughly investigated. In this study, BV2 microglial cells were stimulated with interferon-gamma and lipopolysaccharide and treated with GYY4137. The agent did not influence the viability of BV2 cells in concentrations up to 200 μM. It inhibited tumor necrosis factor but not interleukin-6 production. Expression of CD40 and CD86 were reduced under the influence of the donor. The phagocytic ability of BV2 cells and nitric oxide production were also affected by the agent. Surprisingly, GYY4137 upregulated generation of reactive oxygen species (ROS) by BV2 cells. The effect was mimicked by another H2S donor, Na2S, and it was not reproduced in macrophages. Our results demonstrate that GYY4137 downregulates inflammatory properties of BV2 cells but increases their ability to generate ROS. Further investigation of this unexpected phenomenon is warranted.

scholarly journals Reactive oxygen species and nitric oxide imbalances lead to in vivo and in vitro arrhythmogenic phenotype in acute phase of experimental Chagas disease

2020 ◽  
Vol 16 (3) ◽  
pp. e1008379 ◽  
Author(s):  
Artur Santos-Miranda ◽  
Julliane Vasconcelos Joviano-Santos ◽  
Grazielle Alves Ribeiro ◽  
Ana Flávia M. Botelho ◽  
Peter Rocha ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Chagas Disease ◽  
Acute Phase ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Correction: Reactive oxygen species and nitric oxide imbalances lead to in vivo and in vitro arrhythmogenic phenotype in acute phase of experimental Chagas disease

2020 ◽  
Vol 16 (10) ◽  
pp. e1009049
Author(s):  
Artur Santos-Miranda ◽  
Julliane Vasconcelos Joviano-Santos ◽  
Grazielle Alves Ribeiro ◽  
Ana Flávia M. Botelho ◽  
Peter Rocha ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Chagas Disease ◽  
Acute Phase ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Galectin-1-deficient mice are protected against Trypanosoma cruzi infection through altered neutrophil migration and production of reactive oxygen species and nitric oxide

2020 ◽  
Author(s):  
Thalita Bachelli Riul ◽  
Helioswilton Sales de Campos ◽  
Djalma de Souza Lima-Junior ◽  
Ana Elisa Caleiro Seixas Azzolini ◽  
Cristina Ribeiro de Barros Cardoso ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Trypanosoma Cruzi ◽  
Neutrophil Migration ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Infection Site ◽  
Neutrophil Accumulation

SUMMARYTrypanosoma cruzi is an intracellular parasite that causes Chagas disease that affects millions of people worldwide. Many cellular and molecular aspects of this neglected disease are not fully understood. Prior studies have shown that galectin-1 (Gal-1), a β-galactoside-binding protein that regulates leukocyte recruitment to the inflammatory site, and promotes T. cruzi infection, but the mechanism is unclear. Here, we report that C57BL/6 mice lacking Gal-1 (Lgals1−/−) exhibited lower parasitemia and higher survival rates than their wildtype (WT) counterparts when infected with T. cruzi Y strain. Two weeks after infection, Lgals1−/− mice displayed greater neutrophil accumulation in infection site and heart tissue than WT mice. In T. cruzi-infected Lgals1−/− mice, infiltrated neutrophils produced increased levels of reactive oxygen species (ROS), while macrophages and neutrophils produced increased levels of nitric oxide (NO), which reduced replication and viability of parasites in vitro and downregulated IL-1β production. Pharmacological inhibition of NADPH oxidase and NO synthase during early in vivo infection reversed the protective effect of Gal-1 deficiency in Lgals1−/− mice. Together, our findings demonstrate that lacking Gal-1 favors neutrophil migration to the infection site and increases production of ROS and NO, thereby controlling the early steps of T. cruzi infection by reducing parasitemia and prolonging survival of infected mice.

Synergistic antioxidant activity of size controllable chitosan-templated Prussian blue nanoparticle

Nanomedicine ◽  
2019 ◽  
Vol 14 (19) ◽  
pp. 2567-2578 ◽  
Author(s):  
Hyeryeon Oh ◽  
Jin Sil Lee ◽  
Daekyung Sung ◽  
Jin Hyung Lee ◽  
Sang Hyun Moh ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Antioxidant Activity ◽  
Prussian Blue ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Water Soluble ◽  
Oxygen Species ◽  
Antioxidant Agents

Aim: Prussian blue nanoparticles (PB NPs) have been reported as excellent antioxidant agents owing to their ability to scavenge reactive oxygen species. However, their poor stability in vivo limits their use in biomedical applications. Materials & methods: In this study, we developed chitosan-templated PB NPs using water-soluble chitosan samples with molecular weights ranging from 3 to 100 kDa, which stabilized the PB NPs and improved their antioxidant activity. Results & conclusion: The chitosan-templated PB NPs coordinated with the optimal chitosan molecular weight had uniform sphere-like particles, improved stability and effective scavenging activity of in vitro reactive oxygen species generation in murine fibroblast cells stimulated by oxidative stress agents without any cytotoxicity, implying that they could be promising antioxidant agents.

Enhanced Effect of Clarithromycin on Neutrophil Function In Vitro

1996 ◽  
Vol 24 (2) ◽  
pp. 185-189 ◽  
Author(s):  
H Akamatsu ◽  
Y Niwa ◽  
H Sasaki ◽  
Y Asada ◽  
T Horio
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
In Vitro Study ◽  
Neutrophil Function ◽  
Vitro Study ◽  
Oxygen Species

An in vitro study was carried out to investigate the effect of clarithromycin, a new oral macrolide, on neutrophil reactive oxygen species generation and chemotaxis. It was found that neutrophil-generated 02−, H202 and OH· levels were significantly increased by clarithromycin at concentrations of 50 μg/ml ( P < 0.05). The drug also significantly increased chemotaxis ( P < 0.05). These results indicate that clarithromycin may enhance the activation of neutrophils in vivo.

scholarly journals Oxidised dextrans influence on reactive oxygen species generation by murine peritoneal exudate phagocytic cells

2013 ◽  
Vol 59 (1) ◽  
pp. 81-89 ◽  
Author(s):  
V.O. Tkachev ◽  
M.V. Zaikovskaya ◽  
A.V. Troitsky ◽  
N.G. Luzgina ◽  
V.A. Shkurupy
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Phagocytic Cells ◽  
Mitochondrial Potential ◽  
Transmembrane Mitochondrial Potential ◽  
Species Production

The effects of oxidized dextrans of different molecular weight on reactive oxygen species production and transmembrane mitochondrial potential of macrophages and neutrophils have been studied in vivo and in vitro . Oxidised dextrans demonstrated moderate direct antioxidant ability but induced intracellular oxidative stress through the increase of oxygen radical generation. This effect of the investigated compounds amplifies the cytotoxic and bactericidal potential of phagocytes and can influence isoniazid metabolism, thus increasing its efficiency in therapy of infectious diseases.

scholarly journals Targeting autophagy enhances atezolizumab-induced mitochondria-related apoptosis in osteosarcoma

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Zhuochao Liu ◽  
Hongyi Wang ◽  
Chuanzhen Hu ◽  
Chuanlong Wu ◽  
Jun Wang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Antitumor Immunity ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Specific Monoclonal Antibody ◽  
Osteosarcoma Cells ◽  
Jnk Pathway ◽  
In Vivo Experiments

AbstractIn this study, we identified the multifaceted effects of atezolizumab, a specific monoclonal antibody against PD-L1, in tumor suppression except for restoring antitumor immunity, and investigated the promising ways to improve its efficacy. Atezolizumab could inhibit the proliferation and induce immune-independent apoptosis of osteosarcoma cells. With further exploration, we found that atezolizumab could impair mitochondria of osteosarcoma cells, resulting in increased release of reactive oxygen species and cytochrome-c, eventually leading to mitochondrial-related apoptosis via activating JNK pathway. Nevertheless, the excessive release of reactive oxygen species also activated the protective autophagy of osteosarcoma cells. Therefore, when we combined atezolizumab with autophagy inhibitors, the cytotoxic effect of atezolizumab on osteosarcoma cells was significantly enhanced in vitro. Further in vivo experiments also confirmed that atezolizumab combined with chloroquine achieved the most significant antitumor effect. Taken together, our study indicates that atezolizumab can induce mitochondrial-related apoptosis and protective autophagy independently of the immune system, and targeting autophagy is a promising combinatorial approach to amplify its cytotoxicity.

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