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NADPH oxidative activity, ROS and MDA levels in two groups. A. NADPH consumption were enhanced from 5.4 to 10.4 nmol/mg protein/min in EPCs from CAD versus control groups, n=11, 12, *P<0.05. B. ROS production were significantly increased by 63.5% in EPCs from CAD versus control groups, n=13, 15, *P<0.05. C. The concentrations of MDA were elevated by 131% in EPCs from CAD subjects versus control groups, n=14, 17, *P<0.05. D. The main source of ROS in CAD-EPCs. EPCs from CAD subjects were incubated with apocynin (100 μmol/L), L-NAME (1 mmol/L), oxypurinol (100 μmol/L), rotenone (250 μmol/L) and p47 phox siRNA, EPCs from CAD subjects without intervention were used as the control group, n=6 per group. ROS production was significantly reduced in the group of apocynin, L-NAME and p47 phox siRNA (*P<0.05).
Source publication
Objectives:
The study was designed to investigate the oxidative stress levels of endothelial progenitor cells (EPCs) in stable coronary artery disease (CAD) and to explore the underlying mechanisms of NADPH oxidase activation and subsequent EPCs dysfunction.
Methods:
EPCs were isolated from patients with stable CAD (n=50) and matched healthy vol...
Contexts in source publication
Context 2
... of MDA were elevated by 131% in EPCs from CAD subjects (P<0.05) (Figure 1). All of these indicated that the oxidative stress levels of EPCs in stable coronary artery disease were significantly ...
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Citations
... [4][5][6][7] By triggering endothelial activation, oxidative stress causes endothelial dysfunction with a broad spectrum of consequences, such as impaired vasodilation and abnormal vascular reactivity; expression of chemotactic/adhesive molecules; increased platelet activation and thrombus formation; increased vascular permeability; proliferation and migration of smooth muscle cells; monocyte migration, white blood cell adhesion, and impaired regeneration. [7][8][9][10][11][12][13][14][15][16][17][18][19][20][21] In the present study, we aimed to evaluate oxidative and inflammatory statuses in patients with MINOCA and compare them with the same indices of patients with obstructive coronary disease non-ST-elevation acute coronary syndrome (NSTE-ACS). ...
... p47phox regulates the activation of NOX, thereby generating a large amount of ROS [23] . The excessive ROS over scavenging capacity of the body can activate intracellular signaling pathways by increasing calcium ion levels, changing the redox state of cells, and upregulating the expression of inflammatory molecules, promoting smooth muscle cell proliferation and oxidative modification of low-density lipoprotein, causing changes in vasoconstriction, ultimately leading to the occurrence and development of CHD [24,25] . Our results suggested that HSCARG suppressed p47phox expression in in vitro model by NF-κB activity. ...
Introduction:
Coronary heart disease (CHD) is a dynamic process in which there are interactions between endothelial dysfunction, oxidative stress, and inflammatory responses. The aim of the present study was to investigate the function and mechanism of HSCARG in the treatment of CHD.
Methods:
Male apolipoprotein E/low-density lipoprotein receptor-deficient mice were given a high-fat diet with 21% fat and 0.15% cholesterol for the in vivo model. Human umbilical vein endothelial cells were incubated with angiotensin II for the in vitro model. HSCARG expression was inhibited in patients or mice with CHD.
Results:
HSCARG reduced oxidative stress in mice with CHD. HSCARG also reduced reactive oxygen species (ROS)-oxidative stress in the in vitro model. HSCARG induced p47phox expression in the in vitro model by NF-κB activity. The regulation of nuclear factor kappa B (NF-κB) activity or p47phox expression participates in the effects of HSCARG in CHD.
Conclusion:
Altogether, our data indicate that HSCARG reduced ROS-oxidative stress in in vivo and in vitro models of CHD via p47phox by NF-κB activity and may be a clinical target for CHD.
... NADPH oxidase 4 can impair the function of EPCs. NADPH acts as a substrate and is crucial for maintaining cellular redox homeostasis [61]. Oxidative stress can cause endothelial cell injury and EPC dysfunction [62], which promotes pathological changes in coronary heart disease. ...
Vascular injury is a frequent pathology in coronary artery disease. To repair the vasculature, scientists have found that endothelial progenitor cells (EPCs) have excellent properties associated with angiogenesis. Over time, research on EPCs has made encouraging progress regardless of pathology or clinical technology. This review focuses on the origins and cell markers of EPCs, and the connection between EPCs and coronary artery disease. In addition, we summarized various studies of EPC-capturing stents and EPC infusion therapy, and aim to learn from past technology to predict the future.
... In cancer cells, L-serine acts as an input into the folate and methionine cycles and the connected transsulfuration pathway to regulate the expression of glutathione, a regulator of the redox balance in cells through its ability to scavenge ROS and maintain an appropriate NADPH/NADP + ratio (Locasale 2013;Martínez-Reyes and Chandel 2014;Schieber and Chandel 2014). NADPH maintains cellular antioxidant capacity and promotes the production of the ROS scavengers, thioredoxin, and gonadotropin (Zhang et al. 2016). Furthermore, L-serine is known to directly act as a ROS scavenger in some tissues (Maralani et al. 2012), and it could play this role in HEI-OC1 cells. ...
... Even if L-serine treatment causes otoprotective benefits, it could potentially modulate pathways that counteract the anticancer effect of cisplatin. As increased ROS production is associated with cisplatin's cancer cell toxicity (Choi et al. 2015;Teppo et al. 2017), promoting the expression of ROS scavenging molecules (Martínez-Reyes and Chandel 2014; Schieber and Chandel 2014;Zhang et al. 2016) could nullify the effect of cisplatin to kill cancer cells. Furthermore, Lserine treatment could potentially act through the folate and methionine cycles, and associated transsulfuration pathway, to up-regulate glutathione production (Locasale 2013;Martínez-Reyes and Chandel 2014;Schieber and Chandel 2014). ...
Cisplatin is a platinum-based chemotherapy compound effective against a variety of cancers. However, it can cause increased reactive oxygen species (ROS) production in auditory and vestibular tissue leading to permanent hearing and balance loss. The amino acid, L-serine, has been shown to reduce ROS in some tissue types. In this project, we first investigated whether L-serine could reduce cisplatin-mediated ROS generation in zebrafish utricular tissue culture using spectrophotometry and the fluorescent ROS detector dye, H2DCFDA. Then, we examined whether L-serine could prevent the effect of cisplatin against cellular viability in the mouse auditory hybridoma cell line, HEI-OC1, using the spectrophotometric (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) (MTT) assay. As a final step, we used H2DCFDA dye and flow cytometry analysis to determine if L-serine could counteract the effect of cisplatin on ROS production in this cell line. We found that cisplatin and L-serine treatment may influence ROS production in utricular tissue. Further, although L-serine did not counteract the effect of cisplatin against HEI-OC1 cellular viability, the amino acid did prevent the platinum compound’s effect to increase ROS in these cells. These results suggest that L-serine may act in auditory and vestibular tissues as an effective protectant against cisplatin-mediated toxicity.
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One of the novel interesting topics in the study of cardiovascular disease is the role of the oxidation system, since inflammation and oxidative stress are known to lead to cardiovascular diseases, their progression and complications. During decades of research, many complex interactions between agents of oxidative stress, oxidation, and antioxidant systems have been elucidated, and numerous important pathophysiological links to na number of disorders and diseases have been established. This review article will present the most relevant knowledge linking oxidative stress to vascular dysfunction and disease. The review will focus on the role of oxidative stress in endotheleial dysfunction, atherosclerosis, and other pathogenetic processes and mechanisms that contribute to the development of ischemic heart disease.
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Introduction
In the present study, we aimed to explore the functional role of Pellino-1 (Peli1) in inducing neovascularization after myocardial infarction (MI) and hindlimb ischemia (HLI) using Peli1 global knockout mice (Peli1−/−). Recently we have shown that Peli1, an E3 ubiquitin ligase, induce angiogenesis and improve survivability, with decreased necrosis of ischemic skin flaps.
Methods
Peli1fl/fl and Peli1−/− mice were subjected to either permanent ligation of the left anterior descending coronary artery (LAD) or sham surgery (S). Tissues from the left ventricular risk area were collected at different time points post-MI. In addition, Peli1fl/fl and Peli1−/− mice were also subjected to permanent ligation of the right femoral artery followed by motor function scores, Doppler analysis for blood perfusion and immunohistochemical analysis.
Results
Global Peli1 knockout exacerbated myocardial dysfunction, 30 and 60 days after MI compared to wild type (WT) mice as measured by echocardiogram. In addition, Peli1−/− mice also showed decreased motor function scores and perfusion ratios compared with Peli1fl/fl mice 28 days after the induction of HLI. The use of Peli1 in adenoviral gene therapy following HLI in CD1 mice improved the perfusion ratio at 28 days compared to Ad.LacZ-injected mice.
Conclusion
These results suggest new insights into the protective role of Peli1 on ischemic tissues and its influence on survival signaling.
... In CHD, OS may contribute to vascular epithelial injury via the Sirt1/Nrf2 and p38 MAPK pathways [72], as well as the NF-κB/p65 pathway [73]. Moreover, NOX activation facilitates the initiation and progression of coronary artery disease (CAD) through the PKCα/β2 signaling pathway [74]. Similar mechanisms involving active OS action also happens in depression. ...
The public health sector faces a huge challenge as a result of the high prevalence and burden of disability caused by ischemic cardio-cerebrovascular disease (CVD) and depression. Although studies have explored the underlying mechanisms and potential therapies to address conditions, there is no treatment breakthrough, especially for depression which is highly influenced by social stressors. However, accumulating evidence reveals that CVD and depression are correlated and share common risk factors, particularly obesity, diabetes, and hypertension. They also share common mechanisms, including oxidative stress (OS), inflammation and immune response, cell death signaling pathway, and microbiome-gut-brain axis. This review summarizes the relationship between ischemic CVD and depression and describes the interactions among common risk factors and mechanisms for these two diseases. In addition, we propose that OS mediates the crosstalk between these diseases. We also reveal the potential of antioxidants to ameliorate OS-related injuries.
... Zhang Out of all subunits, p47phox and p22phox regulate the activity of NADPH for production of superoxide radicals and hydrogen peroxide. Activation of p47phox occurs when it is translocated from cytosol to plasma membrane of endothelial cells, and it was observed that the activation rate is enhanced in CAD patients (p < 0.05) [53,57]. The genes encoding NOX enzyme subunits are shown in Table 26.2. ...
Coronary artery disease (CAD) remains the leading global public health burden in cardiovascular diseases. Atherosclerosis is a primary mechanism to cause CAD with the contribution of epidemiological, traditional, genetic, and epigenetic risk factors. Statins, prescribed drugs for lowering of cholesterol levels, also have pleiotropic effect on oxidative stress, inflammation, apoptosis, etc. Reactive oxygen species (ROS)-induced oxidative stress associates with risk factors and participates in initiation and progression of disease. ROS molecules generated as superoxides (O2•ˉ), singlet/triplet oxygen, peroxides (H2O2, ONOO⁻), and hydroxyl radicals (HO•) via reactions catalyzed by endothelial nitric oxide synthase, myeloperoxidase, NADPH oxidase, and xanthine oxidase enzyme are encoded by eNOS, MPO, NOX, and XO genes, respectively. Polymorphisms in eNOS, MPO, NOX, and XO genes influence the expression and attributes to interindividual variation in response to statin drugs. Differential response to statin drug insights into emerging of pharmacogenetic studies to understand the genetic makeup and treat the patient with suitable drug and dose. In clinical practice, pharmacogenetic approach toward oxidative stress is a future emerging trend in personalized medicine development.
... The oxidative stress (OS) state is characterized by an increase in the amount of reactive oxygen and nitrogen species that overwhelm the antioxidant defense systems of the body. This state is implicated in the pathophysiology of multiple chronic conditions, including cardiovascular disease (CVD). 1 Inflammation and oxidation play a critical role in the pathophysiology of atherosclerosis leading to CVD. 2,3 Reactive oxygen species (ROS) initiate cellular tissue damage by modifying lipids, proteins, and DNA. Oxidative modification of LDL by free radicals results in negative effects on vascular function such as reduction in nitric oxide (NO) levels, endothelial apoptosis, increase in smooth muscle cell proliferation, and synthesis of proinflammatory molecules. ...
Objective The aim of this study was to investigate the relationship between oxidative and antioxidative stress markers with presence of left ventricular dysfunction (LVD) and the severity of LVD with coronary artery disease (CAD) in patients who have undergone percutaneous coronary intervention (PCI). Further, the role of oxidative and anti-oxidative stress markers on gender was also investigated.
Methods This was an observational prospective pilot study of patients diagnosed with CAD with LVD who underwent PCI at the center from June 2017 to December 2017. Based on the ejection function (EF), patients were categorized into three groups: mild (> 40–50%), moderate (> 35–40%), and severe (≤ 35%). The oxidative and antioxidative stress markers (malondialdehyde [MDA], glutathione [GSH], and nitric oxide [NO]) were studied and compared in these groups and in both genders as subanalysis.
Results Total 33 patients were enrolled, of whom 23 were male (69.7%) and 10 were female (30.3%). Mean age of the study population was 58.8 ± 9.3 years. Significant elevation of MDA and NO was seen in 33 (100%) and 26 (78.8%), respectively, and decreased GSH was seen in 30 (90.9%). There was no significant difference with respect to oxidative and antioxidative stress markers and severity of LVD (MDA, p = 0.25; NO, p = 0.79; and GSH, p = 0.2) despite elevated MDA levels in all patients. The subanalysis was done to see the gender effect with oxidative and antioxidative stress markers (MDA, p = 0.29; NO, p = 0.10; and GSH, p = 0.50), and they all were insignificant.
Conclusion In this study, there was no significant relationship of oxidative and anti-oxidative stress markers on the degree of LVD even though the elevated MDA levels suggestive of increased oxidative stress were seen in all patients. The further analysis of gender in relation to oxidative and antioxidative stress markers was also insignificant.
... Studies have demonstrated that the adipogenesis of bone marrow stromal cells is additionally characterized by a marked increase in the expression of PPARγ, consistent with other lipocyte differentiation models (5,8). The increased expression of PPARγ directly activates or induces the gene expression profile of the majority of adipocyte phenotypes, including fatty acid synthase, glutamic acid 4, acetyl coenzyme A and shuttle enzymes (26). ...
... Control, control group; Model, steroid-induced avascular necrosis of the femoral head model group; Nar, naringin; p-AKT, phosphorylated Rac-α serine/threonine protein kinase; 5 Nar, 5 mg/kg naringin treatment group; 10 Nar, 10 mg/kg naringin treatment group; 20 Nar, 20 mg/kg naringin treatment group. an important role (5). PPARγ is regulated by a variety of cytokines in the regulation of adipocyte formation, and these factors promote increased expression of PPARγ, in order to increase the differentiation of bone marrow fat cells and result in a decrease in the differentiation of bone marrow stromal cells to osteoblasts which eventually results in necrosis of the femoral head (25). ...
Naringin, a flavonoid, is the effective pharmaceutical ingredient of drynaria, with the effects of healing fractures, strengthening bones and promoting kidney function. The aim of the present study was to investigate the potential effect of naringin on steroid‑induced avascular necrosis of the femoral head (SANFH). Treatment with naringin markedly protected against the steroid‑induced decrease in serum osteocalcin levels, and the rate of osteonecrosis in a model of SANFH. In addition, naringin decreased the total cholesterol and low density lipoprotein/high density lipoprotein ratio in the SANFH rabbit. It was observed that naringin markedly inhibited caspase‑3 activity, increased runt‑related transcription factor 2 and transcription factor sp7 mRNA expression, promoted alkaline phosphatase activity and upregulated collagen I, peroxisome proliferator‑activated receptor (PPAR) γ2, neurogenic locus notch homolog protein (Notch), β‑catenin and phosphorylated‑Rac‑α serine/threonine protein kinase protein expression in the SANFH rabbit. The results of the present study demonstrated that naringin protects against SANFH through upregulation of PPARγ2 and activation of the Notch signaling pathway, and may be a useful addition to the treatment options for diseases of the femoral head.
