scholarly journals Changes of parameters of carbonyl-oxidative stress in rats with experimental myocardial ischemia under the influence of doxycycline

2018 ◽  
Vol 76 (2) ◽  
pp. 6-12
Author(s):  
V. Tkachenko ◽  
A. Shevtsova
Keyword(s):  
Oxidative Stress ◽  
Heart Diseases ◽  
Myocardial Damage ◽  
Oxidative Modification ◽  
Biochemical Mechanisms ◽  
Cardioprotective Effects ◽  
Experimental Myocardial Ischemia ◽  
Phenol Ring ◽  
Active Substances ◽  
Cardioprotective Action

Heart diseases, especially acute myocardial infarction (AMI), belong to the most severe illnesses that often lead to death. Despite a large number of studies, the biochemical mechanisms of AMI and post-infarction myocardial remodeling are poorly understood. Carbonyl-oxidative stress (COS) is one of the more important triggers of the post-infarction complications in these patients, so the neutralizing of the intermediates and final products of COS are a perspective direction in the treatment of AMI. Flavonoide antioxidants as well as inhibitors of carbonylation and glycation of proteins shown the cardioprotective effects but their use have some limitations. Recently, new studies have appeared concerning the cardioprotective action of the doxycycline (DC). This tetracycline antibiotic can inhibit matrix metalloproteinases and proteolysis in extracellular matrix. At the same time, the presence of a multiple-substituted phenol ring can provide the ability of DC to neutralize free radicals, so we hypothesized that it can inhibit the COS. This article compares the effects of small (4,2 mg/kg) and of large (16.8 mg/kg) doses of DC with the effects of classical antioxidants, corvitin and aminoguanidine. The COS-markers and activity of antioxidant enzymes were determined in the blood and subcellular heart fractions of the rats with pituitrin-isoproterenol-induced myocardial damage. It has been established that DC exhibits cardioprotective properties, reducing the formation of products of carbonyl and oxidative modification of biomolecules TBA-active substances, fluorescent end products of glycation (fAGE), aldehyde phenylhydrazones (AFH) and ketone phenylhydrazones (CPH), and a more pronounced effect was shown for the low doses of this drug. Simultaneously, the DC activates enzymes of antioxidant protection, first of all, glutathione peroxidase. Effects of small doses of DC are comparable or exceed the action of aminoguanidine and corvitin, so DC can be useful in the treatment of postinfarction heart failure.

scholarly journals The Cardio- and Neuroprotective Effects of Corvitin and 2-Oxoglutarate in Rats with Pituitrin-Isoproterenol-Induced Myocardial Damage

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
V. Tkachenko ◽  
Y. Kovalchuk ◽  
N. Bondarenko ◽  
О. Bondarenko ◽  
G. Ushakova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Diseases ◽  
Myocardial Damage ◽  
Thiobarbituric Acid ◽  
Antioxidant Systems ◽  
Neuroprotective Effects ◽  
Coronary Syndrome ◽  
Urgent Task ◽  
End Products ◽  
Cognitive Activities

Heart diseases, especially acute coronary syndrome (ACS), are among the most severe illnesses that often lead to death. Despite significant advances in the prevention and treatment of ACS, the incidence of the disease and its complications are very serious. The imbalance between pro- and antioxidant systems, the formation of active carbonyl compounds, and the end products of glycation in the blood and tissues are the key moments in the development of heart and neurological disorders leading to a change of behavioral responses. So, the search for antioxidants with cardio- and neuroprotective effects is an urgent task. This study was aimed at evaluating the effects of Corvitin and 2-oxoglutarate on physiological parameters, heart histology, and markers of carbonyl/oxidative stress of rats with pituitrin-isoproterenol-induced myocardial damage (PIMD). Increased sweating, tachycardia, significantly decreased locomotor and exploratory activity, changes of ECG, heart histology, and biochemical changes were observed in the PIMD-group. The administration of Corvitin or 2-OG led to the recovery of locomotor and cognitive activities of the rats, improvement in heart histology, a decrease in the levels of thiobarbituric acid reactive substances, advanced glycated end products, and various changes in the activity of the antioxidant enzymes, 6 days after PIMD. So, Corvitin and exogenous 2-OG show cardio- and neuroprotective effects through the decrease of carbonyl/oxidative stress and regulation of the activity of the antioxidant system.

P717Glucagon-like peptide 1 (GLP-1) improves endothelial dysfunction and vascular inflammation in polymicrobial sepsis induced by cecal ligation and puncture (CLP)

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Steven ◽  
J Helmstaedter ◽  
F Pawelke ◽  
K Filippou ◽  
K Frenies ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Clinical Trials ◽  
Endothelial Dysfunction ◽  
Knockout Mice ◽  
Vascular Inflammation ◽  
Cecal Ligation ◽  
Cecal Ligation And Puncture ◽  
Glucose Levels ◽  
Dpp4 Inhibitor ◽  
Cardioprotective Effects

Abstract Objective Sepsis causes severe hypotension, accompanied by high mortality in the setting of septic shock. LEADER, SUSTAIN-6 and other clinical trials revealed cardioprotective and anti-inflammatory properties of GLP-1 analogs like Liraglutide (Lira). We already demonstrated improved survival by amelioration of disseminated intravasal coagulation (DIC) in lipopolysaccharide (LPS)-induced endotoxemia by inhibition of the GLP-1 degrading enzyme dipeptidylpeptidase-4 (DPP-4). With the present study we aim to investigate the mechanism of protective effects of the GLP-1 analog Lira and the DPP4 inhibitor Linagliptin (Lina) in the clinically relevant sepsis model cecal ligation and puncture (CLP). Methods C57/BL6j and endothelial cell-specific GLP-1 receptor knockout mice (Cdh5crexGLP-1rfl/flmice) were used and sepsis was induced by cecal ligation and puncture (CLP). DPP4 inhibitor (Lina, 5mg/kg/d; 3 days) and GLP-1 analog (Lira, 200μg/kg/d; 3 days) were applied subcutaneously. Aortic vascular function was tested by isometric tension recording. Aorta and heart tissue was used for Western blotting, dot blot and qRT-PCR. Endogenous GLP-1 (7–36 and 9–36) and insulin was determined by ELISA. Blood samples were collected for examination of cell count, oxidative stress and glucose levels. Results Body temperature was increased by CLP and normalized by Lina and Lira. Sham- and Lira- but not Lina-treated septic mice showed low blood glucose levels compared to healthy controls. Acetylcholine-induced (endothelium-dependent) vascular relaxation in aorta was impaired by CLP. This was accompanied by vascular inflammation and elevation of IL-6, iNOS, ICAM-1, and TNF-alpha mRNA levels in aortic tissue. Vascular, cardiac and whole blood oxidative stress were increased by CLP. Furthermore, we detected higher levels of IL-6, 3-nitrotyrosine (3-NT) and 4-hydroxynonenal (4-NHE) in plasma of CLP animals. Lina and Lira reduced oxidative stress and vascular inflammation, which was accompanied by improved endothelial function. In addition, CLP treatment in endothelial specific knockout mice of the GLP-1r strongly induced mortality compared to WT mice, with the effect being strongest in the Lira-treated group. Conclusion The present study demonstrates that Lina (DPP4 inhibitor) and the GLP-1 analog Lira ameliorate sepsis-induced endothelial dysfunction by reduction of vascular inflammation and oxidative stress. Clinical trials like LEADER and SUSTAIN-6 proved that GLP-1 analogs like Lira have cardioprotective effects in T2DM patients. The present study, performed in a clinically relevant model of polymicrobial sepsis, reveals that the known cardioprotective effects of GLP-1 might be translated to other diseases which affect the cardiovascular system like sepsis, underlining the potent anti-inflammatory effects of GLP-1 analogs.

scholarly journals Brown Algae Phlorotannins: A Marine Alternative to Break the Oxidative Stress, Inflammation and Cancer Network

Foods ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1478
Author(s):  
Marcelo D. Catarino ◽  
Sónia J. Amarante ◽  
Nuno Mateus ◽  
Artur M. S. Silva ◽  
Susana M. Cardoso
Keyword(s):  
Oxidative Stress ◽  
Physical Inactivity ◽  
Dietary Habits ◽  
Vegetable Intake ◽  
Fruit And Vegetable Intake ◽  
Bioactive Properties ◽  
Ability To Act ◽  
Pharmaceutical Industries ◽  
Biochemical Mechanisms ◽  
Cancer Network

According to the WHO, cancer was responsible for an estimated 9.6 million deaths in 2018, making it the second global leading cause of death. The main risk factors that lead to the development of this disease include poor behavioral and dietary habits, such as tobacco use, alcohol use and lack of fruit and vegetable intake, or physical inactivity. In turn, it is well known that polyphenols are deeply implicated with the lower rates of cancer in populations that consume high levels of plant derived foods. In this field, phlorotannins have been under the spotlight in recent years since they have shown exceptional bioactive properties, with great interest for application in food and pharmaceutical industries. Among their multiple bioactive properties, phlorotannins have revealed the capacity to interfere with several biochemical mechanisms that regulate oxidative stress, inflammation and tumorigenesis, which are central aspects in the pathogenesis of cancer. This versatility and ability to act either directly or indirectly at different stages and mechanisms of cancer growth make these compounds highly appealing for the development of new therapeutical strategies to address this world scourge. The present manuscript revises relevant studies focusing the effects of phlorotannins to counteract the oxidative stress–inflammation network, emphasizing their potential for application in cancer prevention and/or treatment.

scholarly journals Antioxidants, lysosomes and elements status during the life cycle of sea trout Salmo trutta m. trutta L.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Natalia Kurhaluk ◽  
Halyna Tkachenko
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Muscle Tissue ◽  
Salmo Trutta ◽  
Protein Carbonyl ◽  
Oxidative Modification ◽  
Oxidative Stress Biomarkers ◽  
Development Stages ◽  
Stress Biomarkers ◽  
Element Contents

AbstractThe aim of our study was to elucidate the effects of both development stages (parr, smolt, adult, spawner), and kelt as a survival form and sex (male, female) on the functional stability of the lysosomal complex, biomarkers of oxidative stress, and element contents in the muscle tissue of the sea trout (Salmo trutta m. trutta L.) sampled in the Pomerania region (northern Poland). We have evaluated the maximal activities of lysosomal enzymes (alanyl aminopeptidase, leucyl aminopeptidase, β-N-acetylglucosaminidase, and acid phosphatase), lipid peroxidation level, and protein carbonyl derivatives as indices of muscle tissue degradation. The relationship between lysosomal activity and oxidative stress biomarkers estimated by the lipid peroxidation level and protein carbonyl derivatives was also assessed, as well as the relationships between element levels and oxidative stress biomarkers. Trends of the main effects (i.e., the development stages and sex alone, the interaction of the sex and development stage simultaneously) on oxidative stress biomarkers, lysosomal functioning, and element contents in the muscle tissue were evaluated. The study has shown sex-related relationships between the pro- and antioxidant balance and the tissue type in the adult stage as well as modifications in the lysosomal functioning induced by long-term environmental stress associated with changing the habitats from freshwater to seawater and intense migrations. The highest level of toxic products generated in oxidative reactions and oxidative modification of proteins was noted in both the spawner stage and the kelt form. The holistic model of analysis of all parameters of antioxidant defense in all development stages and sex demonstrated the following dependencies for the level of lipid peroxidation, oxidative modification of proteins, lysosomal activities, and element contents: TBARS > OMP KD > OMP AD > TAC, AcP > NAG > LAP > AAP and Cu > Fe > Ca > Mn > Zn > Mg, respectively.

scholarly journals Mitochondrial Lipid Homeostasis at the Crossroads of Liver and Heart Diseases

2021 ◽  
Vol 22 (13) ◽  
pp. 6949
Author(s):  
Siarhei A. Dabravolski ◽  
Evgeny E. Bezsonov ◽  
Mirza S. Baig ◽  
Tatyana V. Popkova ◽  
Alexander N. Orekhov
Keyword(s):  
Heart Diseases ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Liver Mitochondria ◽  
Atherogenic Dyslipidemia ◽  
Cvd Risk ◽  
Alcoholic Fatty Liver ◽  
Cholesterol Levels ◽  
Mitochondrial Lipid ◽  
Cardioprotective Effects

The prevalence of NAFLD (non-alcoholic fatty liver disease) is a rapidly increasing problem, affecting a huge population around the globe. However, CVDs (cardiovascular diseases) are the most common cause of mortality in NAFLD patients. Atherogenic dyslipidemia, characterized by plasma hypertriglyceridemia, increased small dense LDL (low-density lipoprotein) particles, and decreased HDL-C (high-density lipoprotein cholesterol) levels, is often observed in NAFLD patients. In this review, we summarize recent genetic evidence, proving the diverse nature of metabolic pathways involved in NAFLD pathogenesis. Analysis of available genetic data suggests that the altered operation of fatty-acid β-oxidation in liver mitochondria is the key process, connecting NAFLD-mediated dyslipidemia and elevated CVD risk. In addition, we discuss several NAFLD-associated genes with documented anti-atherosclerotic or cardioprotective effects, and current pharmaceutical strategies focused on both NAFLD treatment and reduction of CVD risk.

Abstract 5676: Elevated Oxidative Stress is Associated with Ventricular Fibrillation Episode in Patients with Brugada Syndrome without SCN5A Mutation

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Masamichi Tanaka ◽  
Keiko Ohgou ◽  
Koji Nakagawa ◽  
Takeshi Tada ◽  
Masato Murakami ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factor ◽  
Ventricular Fibrillation ◽  
Brugada Syndrome ◽  
Endomyocardial Biopsy ◽  
Heart Diseases ◽  
Multivariable Analysis ◽  
Pathophysiological Mechanism ◽  
Normal Heart ◽  
Scn5a Mutation

Background; Brugada Syndrome (BS) is a disease known to cause ventricular fibrillation (VF) with structurally normal heart. Gene mutation (i.e. SCN5A) has been proposed to be related to the development of BS and VF. However, the pathophysiological mechanism associated with VF development without SCN5A mutation has not been studied yet. Oxidative stress is a common disorder that is related to many heart diseases. We have previously demonstrated that oxidative stress is closely linked to the arrhythmic development. Accordingly, we examined 4-hydroxy-2-nonenal (HNE) modified protein, which is a common mediator of oxidative stress in the myocardium, and VF episodes in patients with BS. Methods; We collected sixty-eight BS patients that underwent right ventricular endomyocardial biopsy (66 males, 2 female; mean age 49.0±11.6 years old). VF was documented in 11 and SCN5A mutation was detected in 14 patients. Biopsy samples were processed for histology [Masson’s trichrome staining for fibrosis, immuno staining for CD45, CD68, and HNE modified protein]. All results from histology were compared with VF episodes. We also performed the analysis in VF patients with (n=14) or without SCN5A mutations (n=54). Results: HNE positive area was significantly larger in VF patients [VF(+): 16.3±10.5, VF(−): 9.3±5.7%: P=0.029]. All other parameters (fibrosis area, CD45, and CD68) were not different between the groups. In multivariable analysis, HNE positive area was most important risk factor of VF development in patients without SCN5A mutation (P=0.004). Conclusions ; These data suggested that oxidative stress is associated with VF development in BS patients, especially in patients without SCN5A mutation.

CARDIOPROTECTIVE EFFECTS OF CURCUMIN AGAINST DIABETES AND NICOTINE-COMBINED OXIDATIVE STRESS

2017 ◽  
Vol 14 (6) ◽  
pp. 64-71
Author(s):  
ZEIN Shaban Ibrahim ◽  
Mohamed Mohamed Soliman ◽  
Shawky Mahmoud ◽  
Mustafa Shukry
Keyword(s):  
Oxidative Stress ◽  
Cardioprotective Effects

scholarly journals Trop2 Guarantees Cardioprotective Effects of Cortical Bone-Derived Stem Cells on Myocardial Ischemia/Reperfusion Injury

2018 ◽  
Vol 27 (8) ◽  
pp. 1256-1268 ◽  
Author(s):  
Tianyu Li ◽  
Yunshu Su ◽  
Xiongli Yu ◽  
Durgahee S.A. Mouniir ◽  
Jackson Ferdinand Masau ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Myocardial Ischemia ◽  
Cortical Bone ◽  
Heart Function ◽  
Heart Diseases ◽  
Ischemia Reperfusion ◽  
Promising Therapeutic Approach ◽  
Cardioprotective Effects ◽  
Myocardial Ischemia Reperfusion

Stem cell transplantation represents a promising therapeutic approach for myocardial ischemia/reperfusion (I/R) injury, where cortical bone-derived stem cells (CBSCs) stand out and hold superior cardioprotective effects on myocardial infarction than other types of stem cells. However, the molecular mechanism underlying CBSCs function on myocardial I/R injury is poorly understood. In a previous study, we reported that Trop2 (trophoblast cell-surface antigen 2) is expressed exclusively on the CBSCs membrane, and is involved in regulation of proliferation and differentiation of CBSCs. In this study, we found that the Trop2 is essential for the ameliorative effects of CBSCs on myocardial I/R-induced heart damage via promoting angiogenesis and inhibiting cardiomyocytes apoptosis in a paracrine manner. Trop2 is required for the colonization of CBSCs in recipient hearts. When Trop2 was knocked out, CBSCs largely lost their functions in lowering myocardial infarction size, improving heart function, enhancing capillary density, and suppressing myocardial cell death. Mechanistically, activating the AKT/GSK3β/β-Catenin signaling axis contributes to the essential role of Trop2 in CBSCs-rendered cardioprotective effects on myocardial I/R injury. In conclusion, maintaining the expression and/or activation of Trop2 in CBSCs might be a promising strategy for treating myocardial infarction, I/R injury, and other related heart diseases.

scholarly journals Salidroside pretreatment protects against myocardial injury induced by heat stroke in mice

2019 ◽  
Vol 47 (10) ◽  
pp. 5229-5238
Author(s):  
Guo-dong Chen ◽  
Heng Fan ◽  
Jian-Hua Zhu
Keyword(s):  
Oxidative Stress ◽  
Myocardial Injury ◽  
Troponin I ◽  
Heat Stroke ◽  
Cardiac Injury ◽  
Myocardial Damage ◽  
Thiobarbituric Acid ◽  
Protective Effects ◽  
Creatine Kinase Mb ◽  
Factor Α

Objective To explore the protective effects and mechanisms of salidroside on myocardial injury induced by heat stroke (HS) in mice. Methods We pretreated mice with salidroside for 1 week and then established an HS model by exposure to 41.2°C for 1 hour. We then examined the effects of salidroside on survival. We also assessed the severity of cardiac injury by pathology, and analyzed changes in levels of myocardial injury markers, inflammatory cytokines, and oxidative stress. Results Salidroside pretreatment significantly reduced HS-induced mortality and improved thermoregulatory function. Salidroside also provided significant protection against HS-induced myocardial damage, and decreased the expression levels of cardiac troponin I, creatine kinase-MB, and lactate dehydrogenase. Moreover, salidroside attenuated HS-induced changes in the inflammation markers tumor necrosis factor-α, interleukin (IL)-6, and IL-10, and down-regulated the oxidative stress response indicated by thiobarbituric acid reactant substances, malondialdehyde, reduced glutathione, and superoxide dismutase. Conclusions Salidroside pretreatment protected against HS-induced myocardial damage, potentially via a mechanism involving anti-inflammatory and anti-oxidative effects.

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