76 patients with coronary artery disease who underwent aortocoronary bypass surgery were examined to study the role of paraoxonase, myeloperoxidase, arginase, asymmetric dimethylarginine and nitric oxide in the mechanisms of the pathogenesis of post-pericardiotomy syndrome (PPCS). Patients were divided into two groups: the 1st - patients with coronary artery disease, who did not have PPCS as a result of clinical studies; the 2nd- patients with ischemic heart disease (IHD who were diagnosed with PPCS. The results showed that the postoperative period after coronary artery bypass grafting is associated with inhibition of paraoxonase, activation of myeloperoxidase, increased activity of arginase, nitrite/nitrate level and asymmetric dimethylarginine, and may be accompanied by the development of endothelial dysfunction and increased systemic inflammatory response.
View Article and Find Full Text PDFBackground: The identification of biomarkers of post-traumatic osteoarthritis (PTOA) progression is of clinical importance. The aims of this study were: (1) to assess the abilities of various soluble proinflammatory mediators in plasma to distinguish patients with knee PTOA from controls; (2) to determine the correlations between the mediators in plasma and those mediators in synovial fluid (SF); and (3) to explore the associations of the mediators with radiographic PTOA severity.
Materials And Methods: The concentrations of IL-1β, IL-6, IL-18, TNFα, and leptin were measured using ELISA.
The administration of SkQ1 to rats at the dose of 50 nmol/kg for five days significantly increased the mRNA levels of transcription factor Nrf2 and of Nrf2-controlled genes encoding antioxidant enzymes SOD1, SOD2, CAT, and GPx4, whereas changes in the level of mRNA of SOD3 in the cerebral cortex of the rat brain were not significant. This was accompanied by activation of antioxidant enzymes (SOD, CAT, GPx, and GST) and increase in reduced glutathione concentration. Under oxidative stress induced by hyperoxia (0.
View Article and Find Full Text PDF76 patients with coronary heart disease (who had undergone coronary artery bypass grafting) were examined to investigate the role of pro-inflammatory cytokines and enzymes involved in redox regulation, in the mechanisms of development of systemic inflammatory response syndrome. Patients were divided into 2 groups: 1st - patients with coronary heart disease, who as a result of clinical trials has not been set postpericardiotomy syndrome; 2nd - patients with coronary heart disease who have been diagnosed postpericardiotomy syndrome. The blood plasma of both groups indicated intensification of production of interleukin-6, intrleukin-8, as well as - an imbalance in the peroxiredoxin-1 and glutathione peroxidase.
View Article and Find Full Text PDFThe features of regulation of free radical oxidation in the blood and the synovial fluid have been studied in patients with knee osteoarthritis. The data were obtained from 46 patients with primary knee osteoarthritis (II-III Kellgren-Lawrence grade, aged 63.26 ± 9.
View Article and Find Full Text PDFPost-traumatic knee osteoarthritis patients (n=117) and healthy people (n=94) were investigated to determine the genotypic and allelic frequency distribution of polymorphic loci Т-31С, С+3953Т IL-1β and G-308A TNF-α. The plasma and synovial fluid levels of proinflammatory cytokines IL-1β and TNF-α were measured in 31 patients. The research demonstrated that the blood and synovial fluid levels of IL-1β but not TNF-α were increased in patients with post-traumatic knee osteoarthritis.
View Article and Find Full Text PDFThe study demonstrated that oxidative stress induced by hyperoxia (0.5 MPa for 90 min) resulted in reduction of mRNA levels of transcription factor Nrf2 and Nrf2-induced genes encoding antioxidant enzymes (SOD1, CAT, GPx4) in peripheral blood leukocytes of rats. The changes in gene expression profiles under hyperoxia were accompanied by disbalance of activity of antioxidant enzymes in the leukocytes, namely activation of superoxide dismutase and inhibition of catalase, glutathione peroxidase, and glutathione-S-transferase.
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