Lancemaside A from Codonopsis lanceolata prevents hypertension by inhibiting NADPH oxidase 2‐mediated MAPK signalling and improving NO bioavailability in rats

2019 ◽  
Vol 71 (9) ◽  
pp. 1458-1468 ◽  
Author(s):  
You Kyoung Shin ◽  
A Young Han ◽  
Yu Shan Hsieh ◽  
Soonho Kwon ◽  
Jinhye Kim ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Codonopsis Lanceolata ◽  
Lancemaside A ◽  
Mapk Signalling ◽  
No Bioavailability ◽  
Nadph Oxidase 2

scholarly journals NADPH Oxidase 2-Mediated Insult in the Auditory Cortex of Zucker Diabetic Fatty Rats

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Zheng-De Du ◽  
Wei Wei ◽  
Shukui Yu ◽  
Qing-Ling Song ◽  
Ke Liu ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Nadph Oxidase ◽  
Auditory Cortex ◽  
Auditory System ◽  
Auditory Brainstem ◽  
Secondary Symptom ◽  
Zucker Diabetic Fatty Rats ◽  
Brainstem Response ◽  
Zdf Rats ◽  
Nadph Oxidase 2

Clinical data has confirmed that auditory impairment may be a secondary symptom of type 2 diabetes mellitus (T2DM). However, mechanisms underlying pathologic changes that occur in the auditory system, especially in the central auditory system (CAS), remain poorly understood. In this study, Zucker diabetic fatty (ZDF) rats were used as a T2DM rat model to observe ultrastructural alterations in the auditory cortex and investigate possible mechanisms underlying CAS damage in T2DM. The auditory brainstem response (ABR) of ZDF rats was found to be markedly elevated in low (8 kHz) and high (32 kHz) frequencies. Protein expression of NADPH oxidase 2 (NOX2) and its matching subunits P22phox, P47phox, and P67phox was increased in the auditory cortex of ZDF rats. Expression of 8-hydroxy-2-deoxyguanosine (8-OHdG), a marker of DNA oxidative damage, was also increased in the neuronal mitochondria of the auditory cortex of ZDF rats. Additionally, decreases in the mitochondrial total antioxidant capabilities (T-AOC), adenosine triphosphate (ATP) production, and mitochondrial membrane potential (MMP) were detected in the auditory cortex of ZDF rats, suggesting mitochondrial dysfunction. Transmission electron microscopy results indicated that ultrastructural damage had occurred to neurovascular units and mitochondria in the auditory cortex of ZDF rats. Furthermore, cytochrome c (Cyt c) translocation from mitochondria to cytoplasm and caspase 3-dependent apoptosis were also detected in the auditory cortex of ZDF rats. Consequently, the study demonstrated that T2DM may cause morphological damage to the CAS and that NOX2-associated mitochondrial oxidative damage and apoptosis may be partly responsible for this insult.

The depletion of p38alpha kinase upregulates NADPH oxidase 2/NOX2/gp91 expression and the production of superoxide in mouse embryonic stem cells

2019 ◽  
Vol 671 ◽  
pp. 18-26 ◽  
Author(s):  
Lucia Binó ◽  
Iva Veselá ◽  
Iva Papežíková ◽  
Jiřina Procházková ◽  
Ondřej Vašíček ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Nadph Oxidase ◽  
Embryonic Stem ◽  
Mouse Embryonic Stem Cells ◽  
Nadph Oxidase 2

Transient NADPH oxidase 2-dependent H2O2 production drives early palmitate-induced lipotoxicity in pancreatic islets

2021 ◽  
Vol 162 ◽  
pp. 1-13
Author(s):  
Eloisa Aparecida Vilas-Boas ◽  
Lisa Nalbach ◽  
Emmanuel Ampofo ◽  
Camila Ferraz Lucena ◽  
Léa Naudet ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Pancreatic Islets ◽  
H2o2 Production ◽  
Nadph Oxidase 2

scholarly journals NADPH Oxidase 2 Mediates Myocardial Oxygen Wasting in Obesity

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 171 ◽  
Author(s):  
Anne D. Hafstad ◽  
Synne S. Hansen ◽  
Jim Lund ◽  
Celio X. C. Santos ◽  
Neoma T. Boardman ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Mitochondrial Function ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Mechanical Efficiency ◽  
Ros Production ◽  
Knock Out ◽  
Obesity And Diabetes ◽  
Mitochondrial Ros ◽  
Nadph Oxidase 2 ◽  
Knock Out Mice

Obesity and diabetes are independent risk factors for cardiovascular diseases, and they are associated with the development of a specific cardiomyopathy with elevated myocardial oxygen consumption (MVO2) and impaired cardiac efficiency. Although the pathophysiology of this cardiomyopathy is multifactorial and complex, reactive oxygen species (ROS) may play an important role. One of the major ROS-generating enzymes in the cardiomyocytes is nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2), and many potential systemic activators of NOX2 are elevated in obesity and diabetes. We hypothesized that NOX2 activity would influence cardiac energetics and/or the progression of ventricular dysfunction following obesity. Myocardial ROS content and mechanoenergetics were measured in the hearts from diet-induced-obese wild type (DIOWT) and global NOK2 knock-out mice (DIOKO) and in diet-induced obese C57BL/6J mice given normal water (DIO) or water supplemented with the NOX2-inhibitor apocynin (DIOAPO). Mitochondrial function and ROS production were also assessed in DIO and DIOAPO mice. This study demonstrated that ablation and pharmacological inhibition of NOX2 both improved mechanical efficiency and reduced MVO2 for non-mechanical cardiac work. Mitochondrial ROS production was also reduced following NOX2 inhibition, while cardiac mitochondrial function was not markedly altered by apocynin-treatment. Therefore, these results indicate a link between obesity-induced myocardial oxygen wasting, NOX2 activation, and mitochondrial ROS.

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