scholarly journals LEPTIN AS AN INDUCER OF INFLAMMATION AND OXIDATIVE STRESS BY METABOLIC SYNDROME

2014 ◽  
Vol 13 (1) ◽  
pp. 20-26 ◽  
Author(s):  
I. D. Bespalovа
Keyword(s):  
Reactive Oxygen Species ◽  
Metabolic Syndrome ◽  
Essential Hypertension ◽  
Blood Serum ◽  
Systemic Inflammation ◽  
Reactive Oxygen ◽  
Stage Ii ◽  
Mononuclear Leukocytes ◽  
Oxygen Species ◽  
Spontaneous Production

Object of research: to explore the relationship of leptin level in blood serum with markers of systemic inflammation and spontaneous production of cytokines and reactive oxygen species by blood mononuclear leukocytes at metabolic syndrome.Material and methods. We conducted a study of 50 patients with essential hypertension stage II in conjunction with the metabolic syndrome. Along with a complete clinical, laboratory and instrumental examination adopted in specialized cardiological clinic, were determined the concentration of markers of systemic inflammation and leptin in blood serum, as well as the relative abundance of the surface markers CD4+-, CD8+-lymphocytes and CD36+-monocytes, the level of spontaneous production of proand antiinflammatory cytokines and active oxygen species by blood mononuclear leukocytes.Results. It was found that patients with essential hypertension stage II with the MS having hyperleptinemia statistically significantly differ both as greater activity of systemic inflammation, and have a greater percentage of CD4+-lymphocytes and a higher level of spontaneous production of blood mononuclear leukocytes a number of proinflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α, MCP-1) and reactive oxygen species.

Increased Generation of Vascular Reactive Oxygen Species by Ang II Is Mediated Via Src-Dependent Pathways in Essential Hypertension.

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 685-685
Author(s):  
Rhian M Touyz ◽  
Ernesto L Schiffrin
Keyword(s):  
Reactive Oxygen Species ◽  
Essential Hypertension ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Leucine Incorporation ◽  
Oxygen Species ◽  
Ang Ii ◽  
Growth Responses ◽  
Hypertensive Patients ◽  
In Cells

42 We tested the hypothesis that augmented Ang II-induced vascular smooth muscle cell (VSMC) growth in human hypertension is mediated via Src-dependent pathways that generate reactive oxygen species (ROS). VSMCs from arteries of normotensive and hypertensive subjects were studied. Production of ROS was measured by fluorescence digital imaging using dichlorofluorescin diacetate (6 μM). The roles of Src and NADH/NADPH oxidase were assessed with the specific inhibitors, PP2 (10 μM) and diphenylene iodinium (DPI) (10 μM) respectively. c-Src phosphorylation was determined by western blot and kinase activity was assessed by measuring enolase phosphorylation. Ang II increased DCFDA fluorescence. This effect was inhibited by catalase, indicating that the signal was derived predominantly from H 2 O 2 . Ang II increased H 2 O 2 production within 40 minutes. Responses were greater (p<0.05) in cells from hypertensive patients (E max =82±nM) than normotensive subjects (E max = 67±nM). DPI and PP2, but not PP3 (inactive analogue) attenuated (p<0.05) Ang II-induced H 2 O 2 production. PP2 effects were greater in cells from hypertensive patients (delta H 2 O 2 , 28±5nM) vs controls (delta H 2 O 2 , 16±2nM). Ang II increased c-Src phosphorylation and activity, with responses 3-4 fold higher in hypertensives. DPI and PP2 (p<0.01) attenuated Ang II-induced DNA and protein synthesis, as measured by 3 H-thymidine and 3 H-leucine incorporation respectively. Growth responses in hypertensive patients were normalized by PP2. In VSMCs from hypertensive patients, Ang II-induced generation of ROS and growth are augmented. These effects are mediated, in part, by Src-dependent, NADH/NADPH oxidase-dependent cascades. Thus increased Src activity may be an upstream modulator of redox-sensitive pathways that regulate vascular growth and remodeling in essential hypertension.

scholarly journals PGC-1α, Inflammation, and Oxidative Stress: An Integrative View in Metabolism

2020 ◽  
Vol 2020 ◽  
pp. 1-20 ◽  
Author(s):  
Sergio Rius-Pérez ◽  
Isabel Torres-Cuevas ◽  
Iván Millán ◽  
Ángel L. Ortega ◽  
Salvador Pérez
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Metabolic Syndrome ◽  
Inflammatory Response ◽  
Reactive Oxygen ◽  
High Energy ◽  
Low Grade ◽  
Oxygen Species ◽  
Antioxidant Genes ◽  
Integrative View

Peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α is a transcriptional coactivator described as a master regulator of mitochondrial biogenesis and function, including oxidative phosphorylation and reactive oxygen species detoxification. PGC-1α is highly expressed in tissues with high energy demands, and it is clearly associated with the pathogenesis of metabolic syndrome and its principal complications including obesity, type 2 diabetes mellitus, cardiovascular disease, and hepatic steatosis. We herein review the molecular pathways regulated by PGC-1α, which connect oxidative stress and mitochondrial metabolism with inflammatory response and metabolic syndrome. PGC-1α regulates the expression of mitochondrial antioxidant genes, including manganese superoxide dismutase, catalase, peroxiredoxin 3 and 5, uncoupling protein 2, thioredoxin 2, and thioredoxin reductase and thus prevents oxidative injury and mitochondrial dysfunction. Dysregulation of PGC-1α alters redox homeostasis in cells and exacerbates inflammatory response, which is commonly accompanied by metabolic disturbances. During inflammation, low levels of PGC-1α downregulate mitochondrial antioxidant gene expression, induce oxidative stress, and promote nuclear factor kappa B activation. In metabolic syndrome, which is characterized by a chronic low grade of inflammation, PGC-1α dysregulation modifies the metabolic properties of tissues by altering mitochondrial function and promoting reactive oxygen species accumulation. In conclusion, PGC-1α acts as an essential node connecting metabolic regulation, redox control, and inflammatory pathways, and it is an interesting therapeutic target that may have significant benefits for a number of metabolic diseases.

scholarly journals Reactive Oxygen Species and Dopamine Receptor Function in Essential Hypertension

2009 ◽  
Vol 31 (2) ◽  
pp. 156-178 ◽  
Author(s):  
Chunyu Zeng ◽  
Van Anthony M. Villar ◽  
Peiying Yu ◽  
Lin Zhou ◽  
Pedro A. Jose
Keyword(s):  
Reactive Oxygen Species ◽  
Essential Hypertension ◽  
Dopamine Receptor ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Receptor Function

Effect of somatostatin analog on high-fat diet-induced metabolic syndrome: Involvement of reactive oxygen species

Peptides ◽  
2010 ◽  
Vol 31 (4) ◽  
pp. 625-629 ◽  
Author(s):  
Wu Li ◽  
Yong-Hui Shi ◽  
Rui-li Yang ◽  
Jue Cui ◽  
Ying Xiao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Metabolic Syndrome ◽  
High Fat Diet ◽  
Reactive Oxygen ◽  
Somatostatin Analog ◽  
Oxygen Species ◽  
High Fat

scholarly journals Action of chondroitin sulfate on the level of cytokines and reactive oxygen species in blood serum upon carrageenan-induced inflammation

2017 ◽  
Vol 22 (1) ◽  
pp. 9-11
Author(s):  
K. Dvorshchenko ◽  
M. Ashpin ◽  
O. Korotkyi ◽  
Ye. Torgalo ◽  
T. Falalyeyeva
Keyword(s):  
Reactive Oxygen Species ◽  
Blood Serum ◽  
Chondroitin Sulfate ◽  
Inflammatory Cytokines ◽  
Superoxide Radical ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tnf Α ◽  
Rat Paw ◽  
Pro Inflammatory Cytokines

Increase of concentration of pro-inflammatory cytokines (IL-1β, TNF-α) is fixed in blood serum at carrageenan-induced rat paw inflammation, as well as increase of the content of reactive oxygen species (superoxide radical, hydrogen peroxide). At introduction of the preparation on the basis of chondroitin sulfate the level of pro-inflammatory cytokines and reactive oxygen species in blood serum decreases, while the concentration of IL10 increases in 1,7 times concerning the group of animals with сarrageenan-induced inflammation.

scholarly journals Oxidative stress and tissue hypoxia as factors contributing to the development of prostate and bladder dysfunction in metabolic syndrome

2021 ◽  
Vol 14 (2) ◽  
pp. 14-22
Author(s):  
V.I. Kirpatovsky ◽  
◽  
S.A. Golovanov ◽  
V.V. Drozhzheva ◽  
L.V. Kudryavtseva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Metabolic Syndrome ◽  
Confocal Microscopy ◽  
Functional State ◽  
Oxidant Stress ◽  
Reactive Oxygen ◽  
Tissue Hypoxia ◽  
Male Rats ◽  
Oxygen Species

Introduction. The development of oxidative stress and nonspecific inflammation is one of the leading factors in the development of benign prostatic hyperplasia (BPH) and associated urination disorders in metabolic syndrome (MS). However, the specific mechanisms of these processes are not entirely clear. The purpose of the study. To study the activity of reactive oxygen species production and the functional state of mitochondria in the prostate and bladder and their role in the dysfunction of these organs using an experimental model of MS induction in rats. Material and methods. In 10 adult mongrel male rats MS was induced by keeping them on a high-calorie diet with an increased content of carbohydrates and fats for 3 months. 10 rats kept on a standard vivarium diet served as controls. The development of MS was confirmed by characteristic changes in the biochemical analysis of blood (hyperglycemia, hyperuricemia, dyslipidemia, hyperinsulinemia). In both series of rats, sections of the native prostate and bladder were examined by laser confocal microscopy and stained with fluorescent probes that characterize the activity of the production of reactive oxygen species (dichlorofluorescein-DCF) and the functional state of the mitochondria (tetramethylrodamine ether – TMRE). The activity of a number of intracellular enzymes (AST, ALT. Alkaline phosphatase, LDH) was investigated in the tissues and urine. Results. In rats with MS, the development of BPH and hypertrophy of the bladder were revealed, confirmed histologically. The study of sections of both organs by confocal microscopy revealed a significant increase in the production of reactive oxygen species by their cells and a decrease in the functional activity of mitochondria, which indicated the development of oxidant stress and tissue hypoxia. In the prostate, this was accompanied by a decrease in the secretory activity of the prostate glands, and in the bladder – the release of cytoplasmic enzymes from damaged cells into the urine, indicating cell damage. Conclusion. The causes of the development of a non-specific inflammatory process in the prostate and bladder, leading to dysfunction of these organs in MS, are increased production of reactive oxygen species and the development of tissue hypoxia.

scholarly journals The Role of Reactive Oxygen Species in the Pathogenesis of Adipocyte Dysfunction in Metabolic Syndrome. Prospects of Pharmacological Correction

2017 ◽  
Vol 72 (1) ◽  
pp. 11-16 ◽  
Author(s):  
E. S. Prokudina ◽  
L. N. Maslov ◽  
V. V. Ivanov ◽  
I. D. Bespalova ◽  
D. S. Pismennyi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Metabolic Syndrome ◽  
Positive Impact ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tnf Α ◽  
The One

It is established that oxidative stress induces insulin resistance of adipocytes, increases secretion leptin, IL-6, TNF-α by adipocytes. Adiponectin secretion by adipocytes is reduced after the action of reactive oxygen species. Metabolic syndrome contributes to oxidative stress in adipose tissue, on the one hand due to the activation of production of reactive oxygen species by adipocyte NADPH-oxidase, and on the other hand by reducing the antioxidant defense adipocytes. It is found that obesity itself can induce oxidative stress. Chronic stress, glucocorticoids, mineralocorticoids, angiotensin-II, TNF-α play an important role in the pathogenesis of oxidative stress of adipocytes. Metformin remains the cure for the treatment of insulin resistance. The positive results in the treatment of metabolic syndrome by losartan were obtained. Antioxidants and flavonoids exhibit a positive impact on the course of the experimental metabolic syndrome.

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