scholarly journals Hydrogen Sulfide: A Therapeutic Candidate for Fibrotic Disease?

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Kai Song ◽  
Qian Li ◽  
Xiao-Ya Yin ◽  
Ying Lu ◽  
Chun-Feng Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Developed Countries ◽  
Current Data ◽  
Fibrotic Disease ◽  
The Third ◽  
Fibrotic Diseases ◽  
Underlying Mechanisms ◽  
The Developed Countries ◽  
And Oxidative Stress

Fibrotic diseases including chronic kidney disease, liver cirrhosis, idiopathic pulmonary fibrosis, and chronic disease account for 45% mortality in the developed countries and pose a great threat to the global health. Many great targets and molecules have been reported to be involved in the initiation and/or progression of fibrosis, among which inflammation and oxidative stress are well-recognized modulation targets. Hydrogen sulfide (H2S) is the third gasotransmitter with potent properties in inhibiting inflammation and oxidative stress in various organs. Recent evidence suggests that plasma H2S level is decreased in various animal models of fibrotic diseases and supplement of exogenous H2S is able to ameliorate fibrosis in the kidney, lung, liver, and heart. This leads us to propose that modulation of H2S production may represent a promising therapeutic venue for the treatment of a variety of fibrotic diseases. Here, we summarize and discuss the current data on the role and underlying mechanisms of H2S in fibrosis diseases related to heart, liver, kidney, and other organs.

ACS67, a Hydrogen Sulfide–Releasing Derivative of Latanoprost Acid, Attenuates Retinal Ischemia and Oxidative Stress to RGC-5 Cells in Culture

2010 ◽  
Vol 51 (1) ◽  
pp. 284 ◽  
Author(s):  
Neville N. Osborne ◽  
Dan Ji ◽  
Aman S. Abdul Majid ◽  
Rebecca J. Fawcett ◽  
Anna Sparatore ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Retinal Ischemia ◽  
Cells In Culture ◽  
And Oxidative Stress

NaHS inhibits NF-κB signal against inflammation and oxidative stress in post-infectious irritable bowel syndrome

RSC Advances ◽  
2016 ◽  
Vol 6 (69) ◽  
pp. 64208-64214 ◽  
Author(s):  
Shenglan Yang ◽  
Danfang Deng ◽  
Yingying Luo ◽  
Yanran Wu ◽  
Rui Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Irritable Bowel Syndrome ◽  
Hydrogen Sulfide ◽  
Murine Model ◽  
Irritable Bowel ◽  
And Oxidative Stress ◽  
Post Infectious

In this study, the alleviating role of hydrogen sulfide (H2S) was investigated in a Post-Infectious Irritable Bowel Syndrome (PI-IBS) murine model and Caco-2 cells.

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.

INNOVATIONS IN POLICY OF TEACHING AT THE UNIVERSITIES IN THE CONTEXT OF ACADEMIC REVOLUTIONS

2020 ◽  
Keyword(s):  
Higher Education ◽  
Developed Countries ◽  
University Education ◽  
University Teaching ◽  
The European Union ◽  
The Third ◽  
Educational Processes ◽  
The Usa ◽  
The Developed Countries

Categories of the academic revolutions and innovations in a perspective of educational policy at the higher school are considered. Special attention is paid to the development of innovations in training at the foreign and Ukrainian universities, since X1X of a century up to now. It is noted that agricultural, industrial, global, demographic and other revolutions created basis for the academic revolutions which resulted from transformations of society and caused innovations in higher education systems. The contribution of the academic revolutions in strengthening of role of the universities in society is confirmed. The major innovations in training stimulated university teaching throughout all academic revolutionary periods (after 1867, 1945, 1983) in developed industrial and developing countries, such as the USA, some states of the European Union and Ukraine. Emergence of innovations in policy of teaching at the universities during the first academic revolution, their modification during the second one, and new turns in transformation of innovations during the third academic revolution is investigated. Introduction of innovations in teaching differed in intensity and scale during the academic revolutions. On examples of teaching it is shown how political and ideological processes in society influenced functioning of the universities. An attempt to compare educational processes during three revolutions and to reveal the most innovational period was made. It is proved that innovations in training were implanted in three academic revolutions, the third one turned out to be the most innovative. The major innovations in policy of teaching were connected with the development of scientific and technical knowledge that contributed to the emergence of the information society. The developed countries offered the introduction of policy of cooperation in the higher education that made impact on innovations in university education. The Coronavirus pandemic of 2019/20 demonstrated the need to use various forms of Internet communications (Zoom, Google Classroom, Moodle, Whereby, etc.) to switch to new opportunities to teach students in higher education institutions around the world at the beginning of the XXI century.

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.

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.

The Role of Nrf2 in D-Galactose-Induced Cardiac Aging in Mice: Involvement of Oxidative Stress

Gerontology ◽  
2020 ◽  
pp. 1-10
Author(s):  
Xilan Yang ◽  
Jian Jia ◽  
Ling Ding ◽  
Zhen Yu ◽  
Chen Qu
Keyword(s):  
Oxidative Stress ◽  
Developed Countries ◽  
Antioxidative Effect ◽  
Cardiac Aging ◽  
Detailed Mechanism ◽  
Candidate Drug ◽  
Nrf2 Activator ◽  
And Oxidative Stress ◽  
Aging Cell

<b><i>Introduction:</i></b> Cardiac aging is the major risk factor for advanced heart disease, which is the leading cause of death in developed countries, accounting for &#x3e;30% of deaths worldwide. <b><i>Objective:</i></b> To discover the detailed mechanism of cardiac aging and develop an effective therapeutic candidate drug to treat or delay cardiac aging. <b><i>Methods:</i></b> We used D-galactose to induce cardiac aging in Nrf2<sup>+/+</sup> and Nrf2<sup>–/–</sup> mice, and then treated these mice with vehicle or the Nrf2 activator, CDDO-imidazolide (CDDO-Im). <b><i>Results and Conclusions:</i></b> D-galactose injection significantly induced cardiac aging, cell apoptosis, and oxidative stress in Nrf2<sup>+/+</sup> mice, all of which were further exacerbated in Nrf2<sup>–/–</sup> mice. CDDO-Im treatment can effectively weaken oxidative stress and enhance the activities of antioxidant enzymes, but CDDO-Im lost its antioxidative effect in the Nrf2<sup>–/–</sup> mice. Nrf2 activator CDDO-Im could therefore effectively protect against D-galactose-induced cardiac aging by inhibiting oxidative stress, suggesting that CDDO-Im might be a potential and promising therapeutic candidate drug to treat cardiac aging.

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