Soyasaponin Bb inhibits the recruitment of toll-like receptor 4 (TLR4) into lipid rafts and its signaling pathway by suppressing the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-dependent generation of reactive oxygen species

2016 ◽  
Vol 60 (7) ◽  
pp. 1532-1543 ◽  
Author(s):  
Yajie Zhang ◽  
Fengping Chen ◽  
Jiading Chen ◽  
Suqun Huang ◽  
Junbin Chen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Signaling Pathway ◽  
Lipid Rafts ◽  
Nicotinamide Adenine Dinucleotide ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Nicotinamide Adenine ◽  
Oxygen Species ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4

scholarly journals Propofol Limits Microglial Activation after Experimental Brain Trauma through Inhibition of Nicotinamide Adenine Dinucleotide Phosphate Oxidase

2013 ◽  
Vol 119 (6) ◽  
pp. 1370-1388 ◽  
Author(s):  
Tao Luo ◽  
Junfang Wu ◽  
Shruti V. Kabadi ◽  
Boris Sabirzhanov ◽  
Kelsey Guanciale ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Nicotinamide Adenine Dinucleotide ◽  
Microglial Activation ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Interferon Γ ◽  
Oxygen Species ◽  
Neuroprotective Effects

Abstract Background: Microglial activation is implicated in delayed tissue damage after traumatic brain injury (TBI). Activation of microglia causes up-regulation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, with the release of reactive oxygen species and cytotoxicity. Propofol appears to have antiinflammatory actions. The authors evaluated the neuroprotective effects of propofol after TBI and examined in vivo and in vitro whether such actions reflected modulation of NADPH oxidase. Methods: Adult male rats were subjected to moderate lateral fluid percussion TBI. Effect of propofol on brain microglial activation and functional recovery was assessed up to 28 days postinjury. By using primary microglial and BV2 cell cultures, the authors examined propofol modulation of lipopolysaccharide and interferon-γ–induced microglial reactivity and neurotoxicity. Results: Propofol improved cognitive recovery after TBI in novel object recognition test (48 ± 6% for propofol [n = 15] vs. 30 ± 4% for isoflurane [n = 14]; P = 0.005). The functional improvement with propofol was associated with limited microglial activation and decreased cortical lesion volume and neuronal loss. Propofol also attenuated lipopolysaccharide- and interferon-γ–induced microglial activation in vitro, with reduced expression of inducible nitric oxide synthase, nitric oxide, tumor necrosis factor-α, interlukin-1β, reactive oxygen species, and NADPH oxidase. Microglial-induced neurotoxicity in vitro was also markedly reduced by propofol. The protective effect of propofol was attenuated when the NADPH oxidase subunit p22phox was knocked down by small interfering RNA. Moreover, propofol reduced the expression of p22phox and gp91phox, two key components of NADPH oxidase, after TBI. Conclusion: The neuroprotective effects of propofol after TBI appear to be mediated, in part, through the inhibition of NADPH oxidase.

scholarly journals Hydrophilic Tetraphenylethene-Based Tetracationic Cyclophanes: NADPH Recognition and Cell Imaging With Fluorescent Switch

2021 ◽  
Vol 9 ◽  
Author(s):  
Dan Wu ◽  
Zhankui Zhang ◽  
Xinyang Yu ◽  
Bing Bai ◽  
Shaolong Qi
Keyword(s):  
Reactive Oxygen Species ◽  
High Resolution ◽  
Tumor Cells ◽  
Nicotinamide Adenine Dinucleotide ◽  
Cell Imaging ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Nicotinamide Adenine ◽  
Oxygen Species ◽  
Fluorescent Switch ◽  
Antioxidative Ability

A hydrophilic TPE-based tetracationic cyclophane TPE-cyc was synthesized, which could capture intracellular Nicotinamide adenine dinucleotide phosphate and fuel the antioxidative ability of tumor cells to detoxify reactive oxygen species (ROS). Meanwhile, upon the reduction by cellular GSH, TPE-cyc could light up tumor cells, acting as a GSH-responsive fluorescent switch to image cells with high resolution.

scholarly journals Wear Particles Promote Reactive Oxygen Species-Mediated Inflammation via the Nicotinamide Adenine Dinucleotide Phosphate Oxidase Pathway in Macrophages Surrounding Loosened Implants

2015 ◽  
Vol 35 (5) ◽  
pp. 1857-1867 ◽  
Author(s):  
Weishen Chen ◽  
Ziqing Li ◽  
Ying Guo ◽  
Yuhuan Zhou ◽  
Ziji Zhang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nicotinamide Adenine Dinucleotide ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Nicotinamide Adenine ◽  
Ros Generation ◽  
Wear Particles ◽  
Oxygen Species ◽  
Prosthesis Loosening ◽  
Ti Particles

Background/Aims: Prosthesis loosening is closely associated with chronic inflammatory cytokine secretion by macrophages, which are activated by wear particles or inflammatory stimulants such as lipopolysaccharide (LPS). Reactive oxygen species (ROS) are critical regulators of inflammation, but their enzymatic sources in response to wear particles and their effects on peri-implant LPS-tolerance remain unclear. Methods: Three ROS-related enzymes—nicotinamide adenine dinucleotide phosphate oxidase (NOX)-1 and -2 and catalase—were investigated in interface membrane tissues and in titanium (Ti) particle-stimulated macrophages in vitro. The generation of ROS and downstream inflammatory effects were measured with or without pre-incubation with apocynin, an NOX inhibitor. Results: Pre-exposure to Ti particles attenuated NF-κB activation in LPS-stimulated macrophages, indicating that wear particles suppress immune response, which may lead to chronic inflammation. NOX-1 and -2 were highly expressed in aseptically loosened interface membranes and in macrophages stimulated with Ti particles; the particles induced a moderate amount of ROS generation, NF-κB activation, and TNF-a secretion in macrophages, and these effects were suppressed by apocynin. Conclusion: Wear particles induce ROS generation through the NOX signaling pathway, resulting in persistent inflammation and delayed loosening. Thus, the suppression of NOX activity may be a useful strategy for preventing prosthesis loosening.

scholarly journals Diabetes Mellitus Increases Reactive Oxygen Species Production in the Thyroid of Male Rats

Endocrinology ◽  
2013 ◽  
Vol 154 (3) ◽  
pp. 1361-1372 ◽  
Author(s):  
Maria C. S. Santos ◽  
Ruy A. N. Louzada ◽  
Elaine C. L. Souza ◽  
Rodrigo S. Fortunato ◽  
Andressa L. Vasconcelos ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Protein Kinase ◽  
Nicotinamide Adenine Dinucleotide ◽  
Thyroid Disease ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Nicotinamide Adenine ◽  
H2o2 Production ◽  
Oxygen Species

Abstract Diabetes mellitus (DM) disrupts the pituitary-thyroid axis and leads to a higher prevalence of thyroid disease. However, the role of reactive oxygen species in DM thyroid disease pathogenesis is unknown. Dual oxidases (DUOX) is responsible for H2O2 production, which is a cosubstrate for thyroperoxidase, but the accumulation of H2O2 also causes cellular deleterious effects. Nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) is another member of the nicotinamide adenine dinucleotide phosphate oxidase family expressed in the thyroid. Therefore, we aimed to evaluate the thyroid DUOX activity and expression in DM rats in addition to NOX4 expression. In the thyroids of the DM rats, we found increased H2O2 generation due to higher DUOX protein content and DUOX1, DUOX2, and NOX4 mRNA expressions. In rat thyroid PCCL3 cells, both TSH and insulin decreased DUOX activity and DUOX1 mRNA levels, an effect partially reversed by protein kinase A inhibition. Most antioxidant enzymes remained unchanged or decreased in the thyroid of DM rats, whereas only glutathione peroxidase 3 was increased. DUOX1 and NOX4 expression and H2O2 production were significantly higher in cells cultivated with high glucose, which was reversed by protein kinase C inhibition. We conclude that thyroid reactive oxygen species is elevated in experimental rat DM, which is a consequence of low-serum TSH and insulin but is also related to hyperglycemia per se.

Sign in / Sign up

Export Citation Format

Share Document