scholarly journals DNA origami as a nanomedicine for targeted rheumatoid arthritis therapy through reactive oxygen species and nitric oxide scavenging

2022 ◽  
Author(s):  
Yuxuan Ma ◽  
Zhangwei Lu ◽  
Ye Shi ◽  
Zhe Li
Keyword(s):  
Rheumatoid Arthritis ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Dna Origami ◽  
In Vivo Studies ◽  
Oxygen Species ◽  
Collagen Induced Arthritis ◽  
M1 Macrophages

High levels of reactive oxygen species (ROS) and nitric oxide (NO) generated by M1 macrophages induce inflammation in the development of rheumatoid arthritis (RA). The eliminating of ROS and NO therefore represents an alternative strategy for RA treatment. Because DNA molecules possess ROS- and endogenous NO-scavenging capability, herein, we develop a nanomedicine based on triangular DNA origami nanostructures for targeted RA treatment. We showed that folic acid-modified triangular DNA origami nanostructures (FA-tDONs) could reduce ROS and NO simultaneously inside proinflammatory M1 macrophages, leading to their polarization into anti-inflammatory M2 subtype. Further in vivo studies confirmed that FA-tDONs could actively target inflamed joints in collagen-induced arthritis (CIA) mice, attenuate inflammatory cytokines and alleviate disease progression. This work demonstrated that DNA origami itself could act as a potential nanomedicine for targeted RA treatment.

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

Imaging of Reactive Oxygen Species and Nitric Oxide In Vivo in Plant Tissues

2008 ◽  
pp. 397-409 ◽  
Author(s):  
Luisa M. Sandalio ◽  
María Rodríguez‐Serrano ◽  
María C. Romero‐Puertas ◽  
Luis A. del Río
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Plant Tissues ◽  
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 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.

Noradrenaline Protects In Vivo Rat Heart Against Infarction and Ventricular Arrhythmias Via Nitric Oxide and Reactive Oxygen Species

2011 ◽  
Vol 169 (1) ◽  
pp. 9-15 ◽  
Author(s):  
Alireza Imani ◽  
Mahdieh Faghihi ◽  
Sayyed Shahabeddin Sadr ◽  
Somayeh Sadeghi Niaraki ◽  
Ali Mohammad Alizadeh
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Rat Heart ◽  
Ventricular Arrhythmias ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
In Vivo Rat Heart

Upconversion nanoprobes for efficiently in vitro imaging reactive oxygen species and in vivo diagnosing rheumatoid arthritis

Biomaterials ◽  
2015 ◽  
Vol 39 ◽  
pp. 15-22 ◽  
Author(s):  
Zhaowei Chen ◽  
Zhen Liu ◽  
Zhenhua Li ◽  
Enguo Ju ◽  
Nan Gao ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Reactive Oxygen Species ◽  
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.

Scavenging of Reactive Oxygen Species and Inhibition of the Oxidation of Low Density Lipoprotein by the Aqueous Extraction ofAnoectochilus formosanus

2003 ◽  
Vol 31 (01) ◽  
pp. 25-36 ◽  
Author(s):  
Chun-Ching Shih ◽  
Yueh-Wern Wu ◽  
Wen-Chuan Lin
Keyword(s):  
Reactive Oxygen Species ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Reactive Oxygen ◽  
In Vivo Studies ◽  
Ldl Oxidation ◽  
Low Density ◽  
Dependent Manner ◽  
Oxygen Species

The ability of Anoectochilus formosanus extract (AFE) to react with relevant biological oxidants was evaluated in this study. In addition, its effect on oxidation of low density lipoprotein (LDL) was investigated in vitro and in vivo. AFE could scavenge reactive oxygen species, such as superoxide anion and hydroxyl radical. The study of human LDL oxidation showed that AFE delayed oxidation in a concentration-dependent manner. In vivo studies also showed that oral administration of AFE delayed the oxidation of LDL from hyperlipidemic hamsters. The ability of AFE to scavenge free radicals suggests that it may be a promising anti-atherogenic agent.

scholarly journals High salt intake shifts the mechanisms of flow-induced dilation in the middle cerebral arteries of Sprague-Dawley rats

2018 ◽  
Vol 315 (3) ◽  
pp. H718-H730 ◽  
Author(s):  
Anita Matic ◽  
Ivana Jukic ◽  
Ana Stupin ◽  
Lidija Baric ◽  
Zrinka Mihaljevic ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Cerebral Arteries ◽  
Hypoxia Inducible Factor ◽  
Reactive Oxygen ◽  
High Salt ◽  
Oxygen Species ◽  
Hypoxia Inducible Factor 1Α ◽  
Middle Cerebral Arteries

The goal of the present study was to examine the effect of 1 wk of high salt (HS) intake and the role of oxidative stress in changing the mechanisms of flow-induced dilation (FID) in isolated pressurized middle cerebral arteries of male Sprague-Dawley rats ( n = 15–16 rats/group). Reduced FID in the HS group was restored by intake of the superoxide scavenger tempol (HS + tempol in vivo group). The nitric oxide (NO) synthase inhibitor Nω-nitro-l-arginine methyl ester, cyclooxygenase inhibitor indomethacin, and selective inhibitor of microsomal cytochrome P-450 epoxidase activity N-(methylsulfonyl)-2-(2-propynyloxy)-benzenehexanamide significantly reduced FID in the low salt diet-fed group, whereas FID in the HS group was mediated by NO only. Cyclooxygenase-2 mRNA (but not protein) expression was decreased in the HS and HS + tempol in vivo groups. Hypoxia-inducible factor-1α and VEGF protein levels were increased in the HS group but decreased in the HS + tempol in vivo group. Assessment by direct fluorescence of middle cerebral arteries under flow revealed significantly reduced vascular NO levels and increased superoxide/reactive oxygen species levels in the HS group. These results suggest that HS intake impairs FID and changes FID mechanisms to entirely NO dependent, in contrast to the low-salt diet-fed group, where FID is NO, prostanoid, and epoxyeicosatrienoic acid dependent. These changes were accompanied by increased lipid peroxidation products in the plasma of HS diet-fed rats, increased vascular superoxide/reactive oxygen species levels, and decreased NO levels, together with increased expression of hypoxia-inducible factor-1α and VEGF. NEW & NOTEWORTHY High-salt (HS) diet changes the mechanisms of flow-induced dilation in rat middle cerebral arteries from a combination of nitric oxide-, prostanoid-, and epoxyeicosatrienoic acid-dependent mechanisms to, albeit reduced, a solely nitric oxide-dependent dilation. In vivo reactive oxygen species scavenging restores flow-induced dilation in HS diet-fed rats and ameliorates HS-induced increases in the transcription factor hypoxia-inducible factor-1α and expression of its downstream target genes.

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