scholarly journals Waterpipe Tobacco Smoke Inhalation Triggers Thrombogenicity, Cardiac Inflammation and Oxidative Stress in Mice: Effects of Flavouring

2020 ◽  
Vol 21 (4) ◽  
pp. 1291 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Suhail Al-Salam ◽  
Sumaya Beegam ◽  
Priya Yuvaraju ◽  
Nur Elena Zaaba ◽  
...  
Keyword(s):  
Troponin I ◽  
Cardiac Injury ◽  
Cardiovascular Effects ◽  
Immunohistochemical Analysis ◽  
Underlying Mechanism ◽  
Smoke Inhalation ◽  
Control Group ◽  
Heme Oxygenase 1 ◽  
Cardiac Inflammation ◽  
The Impact

The consumption of water-pipe smoking (WPS) has been promoted by the use of flavoured tobacco. However, little is known about the impact of flavouring on the cardiovascular toxicity induced by WPS inhalation. Here, we compared the cardiovascular effects and underlying mechanism of actions of plain (P) (unflavoured) versus apple-flavoured (AF) WPS (30 minutes/day, 5 days/week for 1 month) in mice. Control mice were exposed to air. Both P- and AF-WPS inhalation induced an increase in systolic blood pressure, thrombogenicity and plasma concentration of fibrinogen and von Willebrand factor. In heart homogenates, AF-WPS inhalation caused an increase of 8-isoprostane and a decrease in the levels of reduced glutathione (GSH) and superoxide dismutase (SOD). Nevertheless, P-WPS decreased only the activity of SOD. The concentrations of tumour necrosis factor α and interleukin 1β were increased only in heart homogenates of mice exposed to AF-WPS. Although both P- and AF-WPS increased the concentration of troponin I in heart homogenates and induced DNA damage, the concentration of cleaved caspase 3 was only increased in mice exposed to AF-WPS. Immunohistochemical analysis of the hearts showed that both P- and AF- WPS inhalation decreased the expression of SOD. Moreover, the expression of nuclear factor erythroid-derived 2-like 2 at nuclear level in the heart was higher in both AF-WPS and P-WPS compared with control group, and the effect observed in AF-WPS group was more significant than that seen in P-WPS group. Likewise, the concentration of heme oxygenase-1 was significantly increased in both P-WPS and AF-WPS groups compared with control group, and the effect seen in AF-group was higher than that observed in P-WPS group. In conclusion, our findings showed that both P- and AF-WPS induce thrombogenicity and cardiac injury, and that this toxicity is potentiated by the presence of flavouring.

scholarly journals Myocardial Injury and Overload among Amateur Marathoners as Indicated by Changes in Concentrations of Cardiovascular Biomarkers

2020 ◽  
Vol 17 (17) ◽  
pp. 6191
Author(s):  
Anna Maria Kaleta-Duss ◽  
Zuzanna Lewicka-Potocka ◽  
Alicja Dąbrowska-Kugacka ◽  
Grzegorz Raczak ◽  
Ewa Lewicka
Keyword(s):  
Natriuretic Peptide ◽  
Troponin I ◽  
Cardiac Injury ◽  
Cardiovascular Effects ◽  
High Sensitivity ◽  
Finish Line ◽  
Fatty Acid Binding ◽  
Intensive Exercise ◽  
Galectin 3 ◽  
The Impact

Marathons continue to grow in popularity among amateurs. However, the impact of intensive exercise on the amateur’s cardiovascular system has not yet been studied. Analysis of the influence of the marathon on kinetics of biomarkers reflecting cardiac injury and overload may bring new insights into this issue. We investigated the effect of running a marathon on the concentrations of high sensitivity cardiac troponin I (hs-cTnI), heart-type fatty acid binding protein (H-FABP), N-terminal proatrial natriuretic peptide (NT-proANP), B-type natriuretic peptide (BNP), growth differentiation factor 15 (GDF-15) and galectin 3 (Gal-3) in the population of male amateur runners. The study included 35 amateur marathoners and followed 3 stages: S1—two weeks prior to the marathon, S2—at the finish line and S3—two weeks after. Blood samples were collected at each stage and analyzed for biomarkers and laboratory parameters. Concentrations of all studied biomarkers were significantly higher at S2, whereas at S3 did not differ significantly compared to S1. Running a marathon by an amateur causes an acute rise in biomarkers of cardiac injury and stress. Whether repetitive bouts of intensive exercise elicit long-term adverse cardiovascular effects in amateur marathoners needs further research.

scholarly journals The Impact of Circulating Mitochondrial DNA on Cardiomyocyte Apoptosis and Myocardial Injury After TLR4 Activation in Experimental Autoimmune Myocarditis

2017 ◽  
Vol 42 (2) ◽  
pp. 713-728 ◽  
Author(s):  
Bangwei Wu ◽  
Huanchun Ni ◽  
Jian Li ◽  
Xinyu Zhuang ◽  
Jinjin Zhang ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Troponin I ◽  
Tissue Injury ◽  
H9c2 Cells ◽  
Autoimmune Myocarditis ◽  
Cardiac Inflammation ◽  
Experimental Autoimmune Myocarditis ◽  
Tlr4 Activation ◽  
The Impact ◽  
Experimental Autoimmune

Background/Aims: Mitochondrial DNA (mtDNA), acting as a newly found ‘danger-associated molecular patterns’ (DAMPs), is released into circulation upon tissue injury and performs as a considerable activator of inflammation and immune response. However, the role of circulating mtDNA in experimental autoimmune myocarditis (EAM) as well as Toll like receptor4 (TLR4) mediated cardiac inflammation and injury remains unknown. Methods: A model of EAM was established in BALB/c mice by immunization with porcine cardiac myosin. Lipopolysaccharide (LPS) was used to stimulate TLR4 activation in EAM mice and H9C2 cells. Results: LPS stimulation significantly aggravated cardiac inflammation and tissue injury in EAM, as demonstrated by increased myocardium inflammatory cell infiltration, and up-regulated inflammatory cytokines and troponin I(TnI) level in serum. Circulating mtDNA level was increased in EAM and TLR4 activation led to a greater elevation, which may be related to Reactive oxygen species (ROS) stress involved mtDNA damage characterized by reduced mtDNA copy number in myocardium tissue. In addition, the expression of Toll like receptor9 (TLR9), a ligand of mtDNA, was significantly up-regulated in the myocardium of EAM and EAM LPS group; meanwhile, TLR9 inhibition by ODN 2088 caused an inhibited apoptosis in LPS treated H9C2 cells. Moreover, in EAM and EAM LPS group, simultaneously giving ODN 2088 treatment significantly ameliorated cardiac inflammation and tissue injury compared with untreated group. Conclusion: Increased circulating mtDNA combined with upregulated TLR9 expression may corporately play a role in EAM as well as TLR4 activation mediated cardiac inflammation and injury.

Abstract 264: Inhibiting Fibronectin Improves Cardiac Function in a Mouse Model of Heart Failure

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Iñigo Valiente-Alandi ◽  
Michelle Nieman ◽  
Burns C. Blaxall
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Cardiac Remodeling ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Control Group ◽  
Genetic Ablation ◽  
Cell Functions ◽  
Control Peptide ◽  
The Impact

Heart failure (HF) is a devastating disease with poor prognosis. Hallmarks of HF include pathological fibrosis, remodeling and reduced function. In response to cardiac injury, cardiac fibroblasts (CF) undergo pathologic transition to a myofibroblast (MF) phenotype, characterized by excess production of collagen and other myocardial extracellular matrix (ECM) components, thus exacerbating HF. The ECM protein fibronectin (FN) plays an essential role in pathologic remodeling of the ECM in HF. FN polymerization tightly regulates the assembly of collagens and promotes cell proliferation, growth, migration and contractility. We hypothesize that inhibiting FN polymerization utilizing novel peptides will attenuate cardiac remodeling by limiting CF activation and fibrosis. To investigate this hypothesis, we administered daily injections of the FN polymerization inhibitory peptide pUR4 into wild type animals after ischemia-reperfusion (IR) injury for 1 week, and hearts were harvested 4 weeks post-IR. Mice receiving pUR4 demonstrated significant improvement in cardiac function compared to control peptide-treated animals. In addition, pUR4-treated animals showed a robust reduction of fibrosis, inflammatory cell infiltration, pro-inflammatory cytokines, apoptosis and hypertrophy. The information gleaned from the in vitro data obtained from isolated CF, from unchallenged or injured hearts, treated with pUR4 or control peptide suggested attenuation in cell migration and proliferation cell functions. To examine the impact of FN genetic ablation in cardiac function and cardiac fibrosis, we investigated the fibroblast-mediated role of FN in pathologic cardiac remodeling utilizing our fibroblast-restricted Periostin mERCremER ;FN Flox/Flox (Periostin FN-KO). Analysis of cardiac function by echocardiography of Periostin-FN-KO 4 weeks post-IR revealed limited cardioprotective effect compare to the control group (FN Flox/Flox ). This data suggest that inhibiting FN polymerization may be cardioprotective following cardiac injury, attenuating the pathological effects of FN overproduction and polymerization in the activated CF after injury. Limiting FN polymerization will possible lead to the generation of novel treatments for HF.

Methionine protects from myocardial ischemia/reperfusion injury

2014 ◽  
Vol 2 (2) ◽  
pp. 87-97
Keyword(s):  
Reperfusion Injury ◽  
Surgical Procedure ◽  
Troponin I ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Treated Group ◽  
Control Group ◽  
Control Groups ◽  
Severity Scores

Ischemia-reperfusion of cardiac tissues may lead to a prominent damage of the myocyte through either necrosis or apoptosis that seems to be the predominant modes of death during this period. In this study, we investigated the effects of L-Methionine in regional ischemia/ reperfusion injury and apoptosis. Dwale-sprague rats were divided into four groups (six rats per group). Sham group, rats were subjected for all surgical procedure without ligation of the left interior descending coronary artery (LAD). Control group, in which LAD was ligated. Control vehicle and L-methionine treated groups, rats pretreated with normal saline and L-methionine (100 mg/kg, IP ), respectively, for 7 days then subjected to the surgical procedure with ligation of LAD for 25 minutes followed by 120 minutes reperfusion. At the end of reperfusion, cardiac tissue TNF-α, IL-1β, IL-6 and ssDNA, as well as plasma cardiac troponin I (cTnI) were measured. It has been found that L-methionine treated group showed significant reduction (P˂0.05) in TNFα, IL-1β, IL-6, ssDNA and cTnI with respect to the control groups. Histopathology study revealed that the treatment with L-methionine significantly (P˂0.05) improved cardiac injury as compared with control groups and the total severity scores showed that the cardiac injury was mild (score 1) in 50.0%, moderate (score 2) in 33.3% and sever (score 3) in 16.7% of L-methionine treated group. It is concluded that L-methionine reduces inflammatory reaction associated with ischemia/reperfusion injury induced by LAD ligation in addition to its reduction for cardiac injury induced by ischemia reperfusion.

scholarly journals Cardiac Inflammation, Oxidative Stress, Nrf2 Expression, and Coagulation Events in Mice with Experimental Chronic Kidney Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Abderrahim Nemmar ◽  
Suhail Al-Salam ◽  
Sumaya Beegam ◽  
Nur Elena Zaaba ◽  
Javed Yasin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Dna Damage ◽  
Kidney Disease ◽  
Troponin I ◽  
The Body ◽  
Control Group ◽  
Cardiac Inflammation ◽  
Nrf2 Expression

Chronic kidney disease (CKD) is known to be associated with cardiovascular dysfunction. Dietary adenine intake in mice is also known to induce CKD. However, in this experimental model, the mechanisms underlying the cardiotoxicity and coagulation disturbances are not fully understood. Here, we evaluated cardiac inflammation, oxidative stress, DNA damage, and coagulation events in mice with adenine (0.2% w / w in feed for 4 weeks)-induced CKD. Control mice were fed with normal chow for the same duration. Adenine increased water intake, urine output, relative kidney weight, the plasma concentrations of urea and creatinine, and the urinary concentrations of kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin. It also decreased the body weight and creatinine clearance, and caused kidney DNA damage. Renal histological analysis showed tubular dilation and damage and neutrophilic influx. Adenine induced a significant increase in systolic blood pressure and the concentrations of troponin I, tumor necrosis factor-α, and interleukin-1β in heart homogenates. It also augmented the levels of markers of lipid peroxidation measured by malondialdehyde production and 8-isoprostane, as well as the antioxidants superoxide dismutase and catalase. Immunohistochemical analysis of the hearts showed that adenine increased the expression of nuclear factor erythroid-derived 2-like 2 by cardiomyocytes. It also caused cardiac DNA damage. Moreover, compared with the control group, adenine induced a significant increase in the number of circulating platelet and shortened the thrombotic occlusion time in pial arterioles and venules in vivo, and induced a significant reduction in the prothrombin time and activated partial thromboplastin time. In conclusion, the administration of adenine in mice induced CKD-associated cardiac inflammation, oxidative stress, Nrf2 expression, and DNA damage. It also induced prothrombotic events in vivo. Therefore, this model can be satisfactorily used to study the cardiac pathophysiological events in subjects with CKD and the effect of drug treatment thereon.

scholarly journals Assessing the effect of concomitant administration of artemether-lumefantrine and ciprofloxacin on some cardiac parameters in Wistar rats: “The remedial role of vitamin E”

2021 ◽  
Vol 17 (1) ◽  
pp. 094-104
Author(s):  
Jessie Idongesit Ndem ◽  
Pamela Udoh Sylvanus ◽  
Utibe Evans Bassey ◽  
Blessing Obinaju Effiong ◽  
Efosa Godwin Ewere
Keyword(s):  
Vitamin E ◽  
Cardiac Function ◽  
Wistar Rats ◽  
Troponin I ◽  
Concomitant Administration ◽  
Control Group ◽  
Group I ◽  
Male Wistar Rats ◽  
The Impact

The effect of Vitamin E on some cardiac parameters following concomitant administration of artemether-lumefantrine (AL) and ciprofloxacin in male Wistar rats was investigated. Thirty-five male Wistar rats weighing between 190 – 220 g, used for the study were randomly divided into seven groups of five animals each. Group I served as the control. Group II - VII were administered; 8 mg/kg body weight (bw) of AL; 7.14 mg/kg bw of Ciprofloxacin; 8 mg/kg bw of AL + 7.14 mg/kg bw of Ciprofloxacin; 8 mg/kg bw of AL + 8.57 IU of Vitamin E; 7.14 mg/kg bw of Ciprofloxacin + 8.57 IU of Vitamin E; and 8 mg/kg bw of AL + 7.14 mg/kg bw of Ciprofloxacin + 8.57 IU of Vitamin E respectively. All the drugs were administered at their therapeutic regimen. Some cardiac parameters investigated include lipid profile, Troponin I, Troponin T, Creatine kinase, Lactate dehydrogenase and aspartate aminotransferase. The result showed significant (p < 0.05) increase in all the parameters of cardiac function when treatment groups were compared with control. The observed increase in cardiac indices were however significantly (p < 0.05) ameliorated in Groups V, VII and VII which were co-administered with Vitamin E compared with Groups II, III and IV which received the test drugs independently. The weights of the heart tissues showed the same trend with the parameters of cardiac function assessed and upon administration of vitamin E. The results obtained suggest the antioxidative role of vitamin E in alleviating the negative effects induced by artemether-lumefantrine and ciprofloxacin combination treatment, which may be from the impact of free radicals that may have been generated by the combined drugs.

scholarly journals IL-13 Alleviates Cardiomyocyte Apoptosis by Improving Fatty Acid Oxidation in Mitochondria

2021 ◽  
Vol 9 ◽  
Author(s):  
Xiaoyu Guo ◽  
Ting Hong ◽  
Shen Zhang ◽  
Yazhong Wei ◽  
Haizhen Jin ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Cardiac Injury ◽  
Underlying Mechanism ◽  
Fatty Acid Uptake ◽  
Acid Oxidation ◽  
High Morbidity ◽  
Acid Uptake ◽  
Cardiac Inflammation ◽  
Promising Target ◽  
Mitochondrial Fatty Acid

Sepsis-induced cardiac injury (SIC) is one of the most common complications in the intensive care unit (ICU) with high morbidity and mortality. Mitochondrial dysfunction is one of the main reasons for SIC, and Interleukin-13 (IL-13) is a master regulator of mitochondria biogenesis. The aim of the present study was to investigate the role of IL-13 in SIC and explore the underlying mechanism. It was found that reactive oxygen species (ROS) production and apoptosis were significantly increased in lipopolysaccharide (LPS)-stimulated primary cardiomyocytes, which was accompanied with obvious mitochondria dysfunction. The results of RNA-sequencing (RNA-seq), mitochondrial membrane potential, fatty acid uptake and oxidation rate suggested that treatment with IL-13 could restore the function and morphology of mitochondria, indicating that it played an important role in protecting septic cardiomyocytes. These findings demonstrated that IL-13 alleviated sepsis-induced cardiac inflammation and apoptosis by improving mitochondrial fatty acid uptake and oxidation, suggesting that IL-13 may prove to be a potential promising target for SIC treatment.

scholarly journals Irbesartan ameliorate inflammatory responses, and apoptosis induced by myocardial ischemia/reperfusion in male rats

2019 ◽  
Vol 7 (2) ◽  
pp. 138-150
Author(s):  
Najah R. Hadi ◽  
Fadhil G. Al-Amran
Keyword(s):  
Myocardial Ischemia ◽  
Troponin I ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Male Rats ◽  
Control Group ◽  
Inflammatory Reactions ◽  
Tnf Α ◽  
Myocardial Ischemia Reperfusion

Myocardial ischemia–reperfusion (I-R) represents a clinically relevant problem associated with thrombolysis, angioplasty and coronary bypass surgery. This study was undertaken to investigate the potential role of Irbesartan in amelioration of myocardial I/R injury induced by ligation of coronary artery (LAD) in a rat model. We are pretreated the animals with Irbesartan 3mg/kg i.p. 30 minutes before ligation of LAD. At the end of experiment (2 h of reperfusion), blood samples were collected from the heart for measurement of plasma level of cardiac troponin I (cTn-I). Compared with the sham group, levels of myocardial TNF-α, IL-1β, IL-6, MCP-1, MIP-1 alpha, and plasma cTn-I were increased (P<0.05). Histologically, all rats in control group showed significant cardiac injury after I-R. Furthermore, rats in control group showed significant apoptosis. Irbesartan significantly counteract the increased in myocardium level of TNF-α, IL-1B, IL-6, MCP-1, MIP-1 alpha, plasma cTn-I and apoptotosis (P<0.05). Histological analysis revealed that Irbesartan markedly reduced the severity of heart injury in the rats underwent LAD ligation procedure. We concluded that Irbesartan may ameliorate myocardial I/R injury in rats via interfering with inflammatory reactions and apoptosis which induced by I/R injury.

scholarly journals Impact of Congestive Heart Failure and Role of Cardiac Biomarkers in COVID-19 patients: A Systematic Review and Meta-Analysis

2020 ◽  
Author(s):  
Tarun Dalia ◽  
Shubham Lahan ◽  
Sagar Ranka ◽  
Prakash Acharya ◽  
Archana Gautam ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Disease Severity ◽  
Troponin I ◽  
Severe Disease ◽  
Cardiac Injury ◽  
Cardiac Biomarkers ◽  
Pooled Data ◽  
Increased Risk ◽  
The Impact

Background: Coronavirus disease 2019 (COVID-19) has been reported to cause worse outcomes in patients with underlying cardiovascular disease, especially in patients with acute cardiac injury, which is determined by elevated levels of high-sensitivity troponin. There is a paucity of data on the impact of congestive heart failure (CHF) on outcomes in COVID-19 patients. Methods: We conducted a literature search of PubMed/Medline, EMBASE, and Google Scholar databases from 11/1/2019 till 06/07/2020, and identified all relevant studies reporting cardiovascular comorbidities, cardiac biomarkers, disease severity, and survival. Pooled data from the selected studies were used for metanalysis to identify the impact of risk factors and cardiac biomarker elevation on disease severity and/or mortality. Results: We collected pooled data on 5,967 COVID-19 patients from 20 individual studies. We found that both non-survivors and those with severe disease had an increased risk of acute cardiac injury and cardiac arrhythmias, our pooled relative risk (RR) was - 8.52 (95% CI 3.63-19.98) (p<0.001); and 3.61 (95% CI 2.03-6.43) (p=0.001), respectively. Mean difference in the levels of Troponin-I, CK-MB, and NT-proBNP was higher in deceased and severely infected patients. The RR of in-hospital mortality was 2.35 (95% CI 1.18-4.70) (p=0.022) and 1.52 (95% CI 1.12-2.05) (p=0.008) among patients who had pre-existing CHF and hypertension, respectively. Conclusion: Cardiac involvement in COVID-19 infection appears to significantly adversely impact patient prognosis and survival. Pre-existence of CHF and high cardiac biomarkers like NT-pro BNP and CK-MB levels in COVID-19 patients correlates with worse outcomes. Keywords: Acute cardiac injury; cardiac arrhythmia; mortality risk; cardiac biomarkers, COVID-19.

Cardiac troponin-I in the serum of infants of diabetic mothers

2003 ◽  
Vol 13 (3) ◽  
pp. 248-252 ◽  
Author(s):  
Bülent Oran ◽  
Lokman Çam ◽  
Osman Başpınar ◽  
Tamer Baysal ◽  
İsmail Reisli ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Cardiac Injury ◽  
Cardiac Troponin I ◽  
Control Group ◽  
Infants Of Diabetic Mothers ◽  
Asymptomatic Patients ◽  
Life Threatening ◽  
Diabetic Mothers

A transient form of hypertrophic cardiomyopathy has been previously described in infants of diabetic mothers. When it occurs, it is generally benign. The purpose of our study was to establish the extent of injury to the cardiomyocytes in symptomatic and asymptomatic patients with and without hypertrophic cardiomyopathy.Thus, we compared 35 consecutive patients to 20 healthy controls, establishing the significance, if any, of differences in cardiac troponin-I and creatine kinase, including its MB-fraction, and seeking to establish the value of these parameters in the diagnosis of cardiac injury. We also determined to levels of glucose and insulin in the serum, and took note of electrocardiographic and echocardiographic investigations. Values were determined at the 1st and 7th days after admission in the patients, while parameters were measured in the control group only on the first day.We found that the levels of cardiac troponin-I in the serum, known to be a marker for cardiac injury, were significantly elevated in symptomatic patients with life-threatening respiratory or haemodynamic distress. We speculate that transient ventricular hypertrophy is neither the cause nor the consequence of damage to the cardiomyocytes. It would be interesting, nonetheless, to determine the relationship, if any, between cardiomyocytic damage and clinical outcome.

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