NADPH Oxidase as a Therapeutic Target for Neuroprotection against Ischaemic Stroke: Future Perspectives

McCann, Sarah; Roulston, Carli L

doi:10.3390/brainsci3020561

Cited by 43 publications

(32 citation statements)

References 226 publications

(389 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The cytosolic complex made up of p47, p67, and p40 phox proteins translocate to the membrane and dock with the membrane subunits in response to stimulation. [59] It is well known that gp91phox protein is the catalytic core of NADPH oxidase and mainly responsible for the formation of ROS in cells. [60] A previous study also showed the upregulation of gp91phox expression was associated with the increase in the activity of NADPH oxidase in response to LPS.…”

Section: Figurementioning

confidence: 99%

A Novel Quinolyl‐Substituted Analogue of Resveratrol Inhibits LPS‐Induced Inflammatory Responses in Microglial Cells by Blocking the NF‐κB/MAPK Signaling Pathways

Hou

Zhang

et al. 2019

Molecular Nutrition Food Res

View full text Add to dashboard Cite

Scope The anti‐neuroinflammatory effect of a novel quinolyl‐substituted analogue of resveratrol (RV01) on lipopolysaccharide (LPS)‐induced microglial activation is investigated, as well as the possible underlying mechanisms. Methods and results Cell viability is measured using an MTT assay. Nitric oxide (NO) release is determined by nitrite assay. The interaction between RV01 and inducible nitric oxide synthase (iNOS) is studied using molecular docking. Free radical scavenging activity and reactive oxygen species (ROS) production are determined by DPPH reduction assay and DCFH‐DA assay. Pretreatment with RV01 (1–30 µm) prior to LPS (1 µg mL–1) stimulation decreased NO release and iNOS expression without observable cytotoxicity. RV01 reduced the mRNA levels and secretion of tumor necrosis factor‐α (TNF‐α) and interleukin‐6 (IL‐6). RV01 also inhibited LPS‐induced ROS production and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation. Furthermore, RV01 decreases the protein expression of toll‐like receptor 4 (TLR4) and inhibits the LPS‐induced activation of the mitogen‐activated protein kinase (MAPK) and nuclear transcription factor‐κB (NF‐κB) signaling pathways. Additionally, conditioned medium from microglia co‐treated with LPS and RV01 alleviates the death of SH‐SY5Y cells induced by conditioned medium from activated N9 microglial cells. Lastly, a mouse neuroinflammation model is further used to confirm the effect of RV01 in vivo. Conclusion These results show that RV01 suppresses microglia‐mediated neuroinflammation and protects neurons from inflammatory damage, which indicates that RV01 has great potential as a nutritional preventive strategy for neuroinflammation‐related diseases.

show abstract

Section: Figurementioning

confidence: 99%

A Novel Quinolyl‐Substituted Analogue of Resveratrol Inhibits LPS‐Induced Inflammatory Responses in Microglial Cells by Blocking the NF‐κB/MAPK Signaling Pathways

Hou

Zhang

et al. 2019

Molecular Nutrition Food Res

View full text Add to dashboard Cite

show abstract

“…Pathogen‐killing respiratory/oxidative bursts by phagocytes are highly reliant on NADPH oxidase 2 (Nox2) whose activity, in turn, is subservient to pH changes. The optimal pH for Nox2 activity falls within ~7.2‐7.5 . Severe acidosis and rapid reverse in the circulating pH, as in highly alkali dialysate, would diminish Nox2 activity, compromising phagocytic capability of circulating and tissue phagocytes that are the principal components of innate immunity and the first line of defense against infection.…”

Section: Major Organ and Systemic Effects Of Acid‐base Alterationsmentioning

confidence: 99%

Acid‐base alterations in ESRD and effects of hemodialysis

Qian

2017

Seminars in Dialysis

View full text Add to dashboard Cite

Acid-base alterations in patients with kidney failure and on hemodialysis (HD) treatment contribute to (1) intradialytic hypercapnia and hypoxia, (2) hemodynamic instability and cardiac arrhythmia, (3) systemic inflammation, and (4) a number of associated electrolyte alterations including potentiating effects of hypokalemia, hypocalcemia and, chronically, soft-tissue and vascular calcification, imparting poor prognosis and mortality. This paper discusses acid-base regulation and pathogenesis of dysregulation in patients with kidney failure. Major organ and systemic effects of acid-base perturbations with a specific focus on kidney failure patients on HD are emphasized, and potential mitigating strategies proposed. The high rate of HDrelated complications, specifically those that can be accounted for by rapid and steep acid-base perturbations imposed by HD treatment, attests to the pressing need for investigations to establish a better dialysis regimen. ----------------------------------------------------------------This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

show abstract

“…H 2 O 2 generated by the DUOX enzymes or by the dismutation of O 2 - can be scavenged by the antioxidants catalase (Cat) or glutathione peroxidase (GPx) and form H 2 O and O 2 , be partially reduced to generate hydroxyl radical (OH) by the Fe 3+ -catalyzed Haber-Weiss and Fenton reactions or react with chloride in a reaction catalyzed by myeloperoxidase, resulting in the formation of hypochlorous acid (HOCl; fig. 4) [121]. …”

Section: Ros/rns Generationmentioning

confidence: 99%

Reactive Oxygen Species in Psoriasis and Psoriasis Arthritis: Relevance to Human Disease

Khmaladze

Nandakumar

Holmdahl³

2015

Int Arch Allergy Immunol

View full text Add to dashboard Cite

Psoriasis (Ps) is a chronic, immune-mediated, skin inflammatory disease affecting up to 3% of the population worldwide. Different environmental triggers initiate this complex multifactorial syndrome. Many individuals affected by Ps (6-26%) develop inflammatory disease in other organs, often in the joints as in psoriasis arthritis (PsA). Animal models that reflect the typical Ps syndrome, including both skin and joint pathology as in Ps and PsA, are valuable tools for dissecting disease pathways leading to clinical manifestations. In this context, we developed a new acute Ps and PsA-like disease model that appears after exposure to Saccharomyces cerevisiae mannan in certain mouse strains. The disease was found to be triggered by mannan-activated macrophages, leading to the activation of a pathogenic interleukin-17 pathway involving innate lymphocytes. Interestingly, the production of reactive oxygen species protected the mice from the triggering of this pathway and ameliorated Ps and PsA development.

show abstract

NADPH Oxidase as a Therapeutic Target for Neuroprotection against Ischaemic Stroke: Future Perspectives

Cited by 43 publications

References 226 publications

A Novel Quinolyl‐Substituted Analogue of Resveratrol Inhibits LPS‐Induced Inflammatory Responses in Microglial Cells by Blocking the NF‐κB/MAPK Signaling Pathways

A Novel Quinolyl‐Substituted Analogue of Resveratrol Inhibits LPS‐Induced Inflammatory Responses in Microglial Cells by Blocking the NF‐κB/MAPK Signaling Pathways

Acid‐base alterations in ESRD and effects of hemodialysis

Reactive Oxygen Species in Psoriasis and Psoriasis Arthritis: Relevance to Human Disease

Contact Info

Product

Resources

About