scholarly journals Aging increases vulnerability to stress-induced depression via upregulation of NADPH oxidase in mice

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Jung-Eun Lee ◽  
Hye-Jin Kwon ◽  
Juli Choi ◽  
Ji-Seon Seo ◽  
Pyung-Lim Han
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Chronic Stress ◽  
Brain Aging ◽  
Aged Mice ◽  
Upstream Regulator ◽  
Underlying Mechanisms ◽  
Old Mice ◽  
And Oxidative Stress ◽  
Young Mice

AbstractBrain aging proceeds with cellular and molecular changes in the limbic system. Aging-dependent changes might affect emotion and stress coping, yet the underlying mechanisms remain unclear. Here, we show aged (18-month-old) mice exhibit upregulation of NADPH oxidase and oxidative stress in the hippocampus, which mirrors the changes in young (2-month-old) mice subjected to chronic stress. Aged mice that lack p47phox, a key subunit of NADPH oxidase, do not show increased oxidative stress. Aged mice exhibit depression-like behavior following weak stress that does not produce depressive behavior in young mice. Aged mice have reduced expression of the epigenetic factor SUV39H1 and its upstream regulator p-AMPK, and increased expression of Ppp2ca in the hippocampus—changes that occur in young mice exposed to chronic stress. SUV39H1 mediates stress- and aging-induced sustained upregulation of p47phox and oxidative stress. These results suggest that aging increases susceptibility to stress by upregulating NADPH oxidase in the hippocampus.

scholarly journals Recurrent insulin-induced hypoglycemia induces AngII and COX2 leading to renal (pro)renin receptor expression and oxidative stress

2017 ◽  
Vol 5 (1) ◽  
pp. 71 ◽  
Author(s):  
Wael Alanazi ◽  
Mohammad Uddin ◽  
Selim Fakhruddin ◽  
Keith Jackson
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Kidney Injury ◽  
Organ Damage ◽  
Day Surgery ◽  
Receptor Expression ◽  
Sprague Dawley ◽  
Subunit Expression ◽  
Renal Biomarker ◽  
And Oxidative Stress

Background: Recurrent insulin-induced hypoglycemia (RIIH) is an avoidable consequence in the therapeutic management of diabetes mellitus. RIIH has been implicated in causing hypertension through an increase in renal and systemic AngII production.Objective: The present study was performed to assess the hypothesis that chronic insulin treatment enhances AngII and COX2 formation which in turn increases (pro) renin receptor (PRR) expression and NADPH oxidase-mediated oxidative stress, leading to renal and cardiac injury.Methods: The present studies were conducted in Male Sprague Dawley rats treated with daily subcutaneous injections of 7u/kg insulin or saline for 14 days. On the 14th day, surgery was performed for treatment infusion (captopril 12mg/kg, NS398 0.3mg/kg or vehicle), and renal interstitial fluid sample and urine collections for biomarker measurements. At the end of the experiments, kidneys and hearts were harvested to evaluate PRR and NOX2 (NADPH oxidase subunit) expression and oxidative stress.Results: We found that RIIH enhanced AngII and COX2 activity, leading to renal PRR expression and NADPH oxidase-induced oxidative stress in the heart and kidney. 8-isoprostane was evaluated as a renal biomarker of oxidative stress, which was induced in insulin treated animals and modulated by captopril and NS398. In addition, there was a slight increase in NGAL, a urinary biomarker of acute kidney injury (AKI), in insulin treated animals when compared to control.Conclusion: These results demonstrate that RIIH induces renal PRR expression and oxidative stress through increasing AngII and COX2 in the heart and kidney, leading to end-organ damage.

scholarly journals Metformin Corrects Glucose Metabolism Reprogramming and NLRP3 Inflammasome-Induced Pyroptosis via Inhibiting the TLR4/NF-κB/PFKFB3 Signaling in Trophoblasts: Implication for a Potential Therapy of Preeclampsia

2021 ◽  
Vol 2021 ◽  
pp. 1-22
Author(s):  
Yang Zhang ◽  
Weifang Liu ◽  
Yanqi Zhong ◽  
Qi Li ◽  
Mengying Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nlrp3 Inflammasome ◽  
Low Dose ◽  
Therapeutic Potential ◽  
Metabolic Phenotypes ◽  
Pyrin Domain ◽  
Underlying Mechanisms ◽  
And Oxidative Stress ◽  
Receptor Family

NOD-like receptor family, pyrin domain-containing protein 3 (NLRP3) inflammasome-mediated pyroptosis is a crucial event in the preeclamptic pathogenesis, tightly linked with the uteroplacental TLR4/NF-κB signaling. Trophoblastic glycometabolism reprogramming has now been noticed in the preeclampsia pathogenesis, plausibly modulated by the TLR4/NF-κB signaling as well. Intriguingly, cellular pyroptosis and metabolic phenotypes may be inextricably linked and interacted. Metformin (MET), a widely accepted NF-κB signaling inhibitor, may have therapeutic potential in preeclampsia while the underlying mechanisms remain unclear. Herein, we investigated the role of MET on trophoblastic pyroptosis and its relevant metabolism reprogramming. The safety of pharmacologic MET concentration to trophoblasts was verified at first, which had no adverse effects on trophoblastic viability. Pharmacological MET concentration suppressed NLRP3 inflammasome-induced pyroptosis partly through inhibiting the TLR4/NF-κB signaling in preeclamptic trophoblast models induced via low-dose lipopolysaccharide. Besides, MET corrected the glycometabolic reprogramming and oxidative stress partly via suppressing the TLR4/NF-κB signaling and blocking transcription factor NF-κB1 binding on the promoter PFKFB3, a potent glycolytic accelerator. Furthermore, PFKFB3 can also enhance the NF-κB signaling, reduce NLRP3 ubiquitination, and aggravate pyroptosis. However, MET suppressed pyroptosis partly via inhibiting PFKFB3 as well. These results provided that the TLR4/NF-κB/PFKFB3 pathway may be a novel link between metabolism reprogramming and NLRP3 inflammasome-induced pyroptosis in trophoblasts. Further, MET alleviates the NLRP3 inflammasome-induced pyroptosis, which partly relies on the regulation of TLR4/NF-κB/PFKFB3-dependent glycometabolism reprogramming and redox disorders. Hence, our results provide novel insights into the pathogenesis of preeclampsia and propose MET as a potential therapy.

scholarly journals Voluntary Aerobic Exercise Destiffens Arteries of Old Mice Via Inhibition of NADPH Oxidase‐ and Superoxide‐Dependent Oxidative Stress

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Jason Samuel Eng ◽  
Bryant Thanh Pham ◽  
Lawrence Cody Johnson ◽  
Rachel A Giosca‐Ryan ◽  
Douglas R Seals ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Aerobic Exercise ◽  
Old Mice

Testosterone induces leucocyte migration by NADPH oxidase-driven ROS- and COX2-dependent mechanisms

2015 ◽  
Vol 129 (1) ◽  
pp. 39-48 ◽  
Author(s):  
Andreia Z. Chignalia ◽  
Maria Aparecida Oliveira ◽  
Victor Debbas ◽  
Randal O. Dull ◽  
Francisco R.M. Laurindo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Risk ◽  
Cardiovascular Diseases ◽  
Nadph Oxidase ◽  
Vascular Disease ◽  
Leucocyte Migration ◽  
And Oxidative Stress

Testosterone triggers leucocyte migration and oxidative stress, important features in inflammation and in the development of cardiovascular diseases. The mechanisms by which testosterone increase cardiovascular risk are unknown. We describe one pathway whereby testosterone can potentially contribute to vascular disease.

Infliximab prevents dysfunction of the vas deferens by suppressing inflammation and oxidative stress in rats with chronic stress

Life Sciences ◽  
2020 ◽  
Vol 250 ◽  
pp. 117545
Author(s):  
Tuğçe Demirtaş Şahin ◽  
Semil Selcen Gocmez ◽  
Gökhan Duruksu ◽  
Yusufhan Yazir ◽  
Tijen Utkan
Keyword(s):  
Oxidative Stress ◽  
Chronic Stress ◽  
Vas Deferens ◽  
And Oxidative Stress

scholarly journals Oxidative Stress, Neuroinflammation and Mitochondria in the Pathophysiology of Amyotrophic Lateral Sclerosis

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 901 ◽  
Author(s):  
Elena Obrador ◽  
Rosario Salvador ◽  
Rafael López-Blanch ◽  
Ali Jihad-Jebbar ◽  
Soraya L. Vallés ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amyotrophic Lateral Sclerosis ◽  
Cell Types ◽  
T Cell Subsets ◽  
Cellular Interactions ◽  
Underlying Mechanisms ◽  
Different Cell Types ◽  
And Oxidative Stress ◽  
Different Levels ◽  
Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a progressive motor neuron (MN) disease. Its primary cause remains elusive, although a combination of different causal factors cannot be ruled out. There is no cure, and prognosis is poor. Most patients with ALS die due to disease-related complications, such as respiratory failure, within three years of diagnosis. While the underlying mechanisms are unclear, different cell types (microglia, astrocytes, macrophages and T cell subsets) appear to play key roles in the pathophysiology of the disease. Neuroinflammation and oxidative stress pave the way leading to neurodegeneration and MN death. ALS-associated mitochondrial dysfunction occurs at different levels, and these organelles are involved in the mechanism of MN death. Molecular and cellular interactions are presented here as a sequential cascade of events. Based on our present knowledge, the discussion leads to the idea that feasible therapeutic strategies should focus in interfering with the pathophysiology of the disease at different steps.

Underlying mechanisms of reactive oxygen species and oxidative stress photoinduced by graphene and its surface-functionalized derivatives

2020 ◽  
Vol 7 (3) ◽  
pp. 782-792 ◽  
Author(s):  
Hongye Yao ◽  
Yang Huang ◽  
Xuan Li ◽  
Xuehua Li ◽  
Hongbin Xie ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Functional Groups ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Underlying Mechanisms ◽  
Transformation Processes ◽  
And Oxidative Stress

Graphene can be modified by different functional groups through various transformation processes in the environment.

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