Creatine Kinase-myocardial Band Research Articles

Luteolin ameliorates rat model of metabolic syndrome-induced cardiac injury by apoptosis suppression and autophagy promotion via NR4A2/p53 regulation

BackgroundReduced cardiac autophagy, inflammation, and apoptosis contribute to cardiovascular complications caused by metabolic syndrome (MetS). It is documented that the nuclear receptor 4A2 (NR4A2) could modulate autophagy and apoptosis in cardiac complications. The aim of this investigation was to assess the therapeutic potential of luteolin, with documented beneficial properties, against MetS-associated cardiac injury.MethodsForty male albino Wistar rats were divided into 5 groups randomly as controls, MetS, and MetS animals treated with luteolin (25, 50, 100 mg/kg ip). The animal’s weight, blood pressure, lipid profile, tolerance to glucose and insulin, and cardiac histopathology were evaluated. Moreover, troponin T, creatine kinase-myocardial band (CK-MB), inflammatory profile (IL-6, IL-1β, TNF-α), transforming growth factor-β1 (TGF-β1), oxidative stress, and matrix metalloproteinase-9 (MMP-9) were analyzed to determine the cardiac state. Cardiac NR4A2 and p53, as well as apoptotic (B-cell leukemia/lymphoma 2 [BCL-2], Caspase [CASP]-3, and CASP-9) and autophagic mediators (Sequestosome-1/p62, Microtubule-associated protein 1 A/1B-light chain 3 [LC3], and Beclin-1) were measured by RT-qPCR and ELISA.ResultsLuteolin remarkably restored MetS-induced biochemical derangements and related cardiac injury via the suppression of apoptosis, inflammation, and stress but promotion of autophagy (p-value < 0.001).ConclusionCurrent findings revealed the promising therapeutical properties of luteolin against MetS-associated cardiovascular risks.

The influence of prolonged aerobic exercise on cardiac, muscular, and renal biomarkers in trained individuals with obesity.

The aim of this study was to investigate the influence of prolonged aerobic exercise on cardiac, muscular and renal inflammatory markers in a group of trained obese men. Seventeen men (aged 40 ± 6years; body mass index [BMI] 31.3 ± 2.8kgm-2, maximal oxygen uptake [V'O2max] 41.5 ± 5.6mlkg-1min-1) ran a half, 30km, or full marathon. Troponin I (cTnI), the n-terminal creatine kinase-myocardial band (CK-MB), pro b-type natriuretic peptide (NT-proBNP), lactate dehydrogenase (LDH), myoglobin, creatinine (CREA) and the estimated glomerular filtration rate (eGFR)were measured before (T0), immediately after (T1) and 3days after the race (T2). The concentrations of cTnI, myoglobin, LDH, CK-MB and CREA significantly increased (P < 0.05), whereas eGRF decreased at T1 (P < 0.05). All the above parameters returned to baseline at T2, except for eGFR, which remained lower than that at T0 (P < 0.05). A positive association was observed between ΔCK-MB (%) and the time spent in Zone 3 during the race (R = 0.686, P = 0.014). The Δmyoglobin (%) was positively correlated with race time, race mean speed and time in Zone 3 (R = 0.574-0.862, P < 0.05). The ∆CREA values were moderately correlated with the race mean HRMAX (%) and time spent in Zone 3 (%) (R = 0.514-0.610; P = 0.05). The ∆eGRF values were moderately inversely correlated with the time spent in Zone 3 (%) (R = - 0.627; P < 0.05). Changes in cardiac, muscular and renal inflammatory markers in trained men with obesity are consistent with those described in the literature in normal-weight individuals. Finally, running parameters, such as running time, average running intensity and time in Zone 3 appear to be responsible for the changes in cardiac, muscular and renal function markers after long-distance running.

VPO1 Promotes Programmed Necrosis of Cardiomyocytes in Rats with Chronic Heart Failure by Upregulating CYLD.

Chronic heart failure (CHF) is a serious cardiovascular condition. Vascular peroxidase 1 (VPO1) is associated with various cardiovascular diseases, yet its role in CHF remains unclear. This research aims to explore the involvement of VPO1 in CHF. CHF was induced in rats using adriamycin, and the expression levels of VPO1 and cylindromatosis (CYLD) were assessed. In parallel, the effects of VPO1 on programmed necrosis in H9c2 cells were evaluated through cell viability assays, lactate dehydrogenase (LDH) level measurements, and analysis of receptor-interacting protein kinase 1/receptor-interacting protein kinase 3/mixed lineage kinase domain-like protein (RIPK1/RIPK3/MLKL) pathway-related proteins. The impact of CYLD on RIPK1 protein stability and ubiquitination was also investigated, along with the interaction between VPO1 and CYLD. Additionally, cardiac structure and function were assessed using echocardiography, Hematoxylin-eosin (HE) staining, Masson staining, and measurements of myocardial injury-related factors, including N-terminal prohormone of brain natriuretic peptide (NT-proBNP), Aspartate aminotransferase (AST), LDH, and creatine kinase-myocardial band (CK-MB). VPO1 expression was upregulated in CHF rats and in H9c2 cells treated with adriamycin. In cellular experiments, VPO1 knockdown improved cell viability, inhibited necrosis and the expression of proteins associated with the RIPK1/RIPK3/MLKL pathway. Mechanistically, VPO1 promoted cardiomyocyte programmed necrosis by interacting with the deubiquitinating enzyme CYLD, which enhanced RIPK1 ubiquitination and degradation, leading to activation of the RIPK1/RIPK3/MLKL signaling pathway. At animal level, overexpression of CYLD counteracted the cardiac failure, cardiac hypertrophy, myocardial injury, myocardial fibrosis, and tissue necrosis caused by VPO1 knockdown. VPO1 exacerbates cardiomyocyte programmed necrosis in CHF rats by upregulating CYLD, which activates the RIPK1/RIPK3/MLKL signaling pathway. Thus, VPO1 may represent a potential therapeutic target for CHF.

A retrospective study on the relationship between plasma β-hydroxybutyric acid levels and short-term prognosis of cardiac function in patients with acute myocardial infarction combined with heart failure

Abstract Background Ketone body metabolism can improve cardiomyocytes metabolism and reduce myocardial oxygen consumption; however, its role in the short-term prognosis of patients with acute myocardial infarction combined with heart failure has not been clearly elucidated. The aim of this study was to investigate the effect of β-hydroxybutyric acid, the main component of ketone bodies, on the short-term prognosis of patients with acute myocardial infarction combined with heart failure. Methods This was a retrospective observational study that enrolled patients admitted to the Qilu Hospital of Shandong University for acute myocardial infarction combined with heart failure between January 1, 2019, and December 31, 2022. According to whether β-hydroxybutyric acid was elevated or not, subjects were divided into a β-hydroxybutyric acid elevated and nonelevated groups, to observe the difference in cardiac function improvement between the two groups. Results This study included a total of 260 patients, of which 170 exhibited elevated levels of β-hydroxybutyric acid. Compared to the patients in the nonelevated group, patients in the elevated β-hydroxybutyric acid group had higher plasma levels of creatine kinase myocardial band and greater Gensini scores. Multivariate logistic regression analysis indicated that an increase in β-hydroxybutyric acid levels (odds ratio: 2.517; 95% confidence intervals: 1.394–4.597; P = 0.002) is an independent protective factor affecting the prognosis of cardiac function in patients with acute myocardial infarction combined with heart failure. Conclusion In patients with acute myocardial infarction combined with heart failure, plasma β-hydroxybutyric acid serves as an independent protective factor for short-term improvement in cardiac function.

Effects of extremely low-frequency (50Hz) electromagnetic fields on vital organs of adult Wistar rats and viability of mouse fibroblast cells.

In recent years, scientific communities have been concerned about the potential health effects of periodic electromagnetic field exposure (≤1h/d). The objective of our study is to determine the impact of extremely low-frequency pulsed electromagnetic fields (ELF-PEMF) (1-3mT, 50Hz) on mouse fibroblast (red fluorescent protein (RFP)-L929) cells and adult Wistar rats to gain a comprehensive understanding of biological effects. We observed that RFP-L929 exhibits no significant changes in cell proliferation and morphology but mild elevation in aspartate aminotransferases, alanine aminotransferases, total bilirubin, serum creatinine, and creatine kinase-myocardial band levels in ELF-PEMF exposed groups under in vitro and in vivo conditions. However, the histological examination showed no significant alterations in tissue structure and morphologies. Our result suggests that 50-Hz ELF-PEMF exposure (1-3mT, 50Hz) with duration (<1h/d) can trigger mild changes in biochemical parameters, but it is insufficient to induce any pathological alterations.

Anti-inflammatory Effect of Commiphora gileadensis L. Induces Cardiovascular Integrity Markers in Male Diabetic Mice

Background Cardiovascular disease continues to be a predominant source of morbidity and mortality globally. Commiphora gileadensis L. is a tree under the genus Commiphora. Purpose To investigate the anti-inflammatory effect of C. gileadensis L. on cardiovascular and its action in maintaining cardiovascular integrity in Type 1 diabetic mice. Methods Fifty male Bagg albino (BALB/c) mice are classified into five groups: control, untreated diabetic, diabetic C. gileadensis L. sap-treated, methanol extract-treated, and acetone extract-treated. For each mouse in five groups body weight, glycated hemoglobin (HbA1c), sodium, potassium, chloride, urea, creatinine, alanine aminotransferase (ALT), lipid profile, aspartate aminotransferase (AST), lactate dehydrogenase (LD), total creatine kinase (CK), creatine kinase-myocardial band (CK-MB), adropin, nitric oxide (NO), endothelin-1, and vascular endothelial growth factor (VEGF) were measured. In addition, total lymphocytes, CD3+, CD4+, CD8+, CD4+ CD25+, and CD8+ CD25+ were measured in all groups. Results Compared to the untreated diabetic group, diabetic groups treated with C. gileadensis L. had significantly increased body weight after 6 months ( p &lt; 0.05). Diabetic mice treated with C. gileadensis L. extracts had significantly lower HbA1c levels than the diabetic untreated group ( p &lt; 0.01). Furthermore, C. gileadensis L. extracts lowered serum urea and creatinine in diabetic mice ( p &lt; 0.05). Triglyceride, cholesterol, and low-density lipoprotein (LDL) were reduced in mice treated with C. gileadensis L. extracts, whereas high-density lipoprotein (HDL) was elevated compared with diabetic untreated mice ( p &lt; 0.01). Serum AST and endothelin-1 were significantly decreased in diabetic groups treated with C. gileadensis L. extracts ( p &lt; 0.05), while adropin and NO increased ( p &lt; 0.01). Diabetic mice treated with C. gileadensis L. extracts had significantly lower LD, total CK, CK-MB, and VEGF levels than the untreated diabetic group ( p &lt; 0.01). In addition, C. gileadensis L. reduces CD3+, CD4+, CD8+, while increases CD4+ CD25+, and CD8+ CD25+ subsets in diabetic mice ( p &lt; 0.0001). Conclusion C. gileadensis L. induces the levels of cardiovascular integrity markers (adropin and NO) and reduces cardiovascular malfunction markers [endothelin-1 (ET-1) and VEGF] in diabetic mice. The observed properties could be attributed to the antioxidant activity of C. gileadensis L. Furthermore, C. gileadensis L. may help in the prevention of atheroma formation by reducing CD4+ and CD8+ and increasing T regulatory cells (CD4+ CD25+ and CD8+ CD25+).

Myocardial Disorders in BDNF-Deficient Rats: Limited Recovery Post-Moderate Endurance Training.

The study aimed to determine whether heterozygous BDNF-deficient (BDNF-knockout, SD-BDNF) rats exhibit pathological changes in the myocardium and to assess whether a 5-week moderate-intensity endurance training program can reverse adverse changes in the heart muscle. Experiments were conducted on four groups of rats: control wild-type, control BDNF knockout, trained wild-type and trained BDNF knockout. Knockout rats were selected due to the presence of symptoms resembling metabolic syndrome in serum and liver while 5-week moderate endurance training was used as an intervention targeted at restoring heart function. Measurements of BDNF/Trk-B concentrations and molecules levels and activities, such as cardiac specific enzymes like creatine kinase and creatine kinase myocardial band, lipids as total cholesterol, low-density lipoprotein and triglycerides, metabolic enzymes including alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase and lactate dehydrogenase and interleukin-1 were carried out in myocardium homogenates. In BDNF-deficient rats, the myocardium showed significantly reduced lipid concentrations, decreased metabolic and cardiac enzyme activity, and elevated Trk-B levels, all of which are indicative of myocardial ischemia or hypoxia. These changes in critical biomarkers were consistent with those earlier observed in the livers of BDNF-deficient rats, suggesting a link between the liver and cardiac function. Moderate endurance training led to an increase in creatine kinase activity in the myocardium of trained rats, suggesting increased production and utilization of energy required for myocardial contraction in trained wild-type and knockout populations of rats. BDNF-deficient rats exhibited numerous myocardial abnormalities, most of which were not reversible after moderate-intensity endurance training. These findings provide a basis for a deeper understanding of the mechanisms underlying myocardial disorders in BDNF-deficient rats, which appear to be a suitable model for studying various aspects of metabolic disorders.

Inpatient Test Utilization and Test Volume Benchmarking: A Q-Probes Study.

Test-ordering practices vary widely between and within health care organizations, and methods used to benchmark test utilization data are unstandardized. To develop and apply standardized methodology to compare inpatient test utilization data submitted by laboratories enrolled in a College of American Pathologists Q-Probes study. Participating laboratories provided inpatient test volumes for 50 designated analytes and total inpatient days for 2019 or a recent 12-month period. Test utilization patterns were characterized by studying test volumes standardized per 1000 inpatient days. Test volume variability used the standardized median absolute deviation; standardized test volumes were evaluated by calculating comparative ranges for each analyte. Standardized test volumes falling outside their respective comparative ranges are referred to as outliers in this study. Volume data were tested for association with stewardship practices and institutional demographics. Methodology using standardized test volume data identified test groups that are commonly used in the inpatient setting and efficiently identified volume outliers. High test volume outliers included creatine kinase myocardial band, free prostate-specific antigen, myoglobin, serotonin release assay, and hepatitis B serologies; no low-volume outliers were observed. Among 33 participants, 13 (39%) had no test volume outliers, while 5 (15%) showed multiple tests (13-34) with comparatively high volumes. No statistically significant relationships were found between stewardship practices and test-ordering patterns. Our approach can be used to measure inpatient test volume data across organizations and for identifying test volumes falling outside of the standardized comparative ranges that may require interventions to change test utilization practices.

Risk factors for left ventricular remodeling after myocardial infarction: A meta-analysis.

This study aimed to assess potential risk factors for left ventricular remodeling (LVR) after acute myocardial infarction (MI). We systematically searched PubMed, the Cochrane Library, MEDLINE, Embase, Web of Science databases CNKI Scholar, VIP, and WanFang databases for all relevant epidemiological studies published up to August 1, 2023. Fixed-effects model or random-effects model was employed to pool the study-specific effect sizes and 95% confidence intervals (CIs). Fifteen studies with a total of 3,093,792 participants were included according to inclusion criteria. Major modifiable risk factors associated with LVR after MI were diabetes (odds ratio [OR] = 2.053, 95% CI: 1.504-2.803), MI site (OR = 2.423, 95% CI: 1.584-3.708), cystatin C (OR = 6.204, 95% CI: 1.830-21.036), B-type natriuretic peptide (OR = 2.280, 95% CI: 1.466-3.546), as well as creatine kinase-myocardial band (OR = 1.013, 95% CI: 0.985-1.042). The current study provides evidence indicating that diabetes, the site of MI, cystatin C, B-type natriuretic peptide, and creatine kinase-myocardial band are the primary risk factors for LVR after MI. Recognizing and addressing these modifiable risk factors is crucial for the development of effective preventive and treatment strategies.

Novel perspectives on early diagnosis of acute compartment syndrome: the role of admission blood tests

PurposeThe role of admission blood indicators in patients with acute compartment syndrome (ACS) remains debated. Our primary purpose was to observe variations of admission blood indicators in patients with ACS, while our secondary goal was to explore potential biomarkers related to ACS.MethodsWe collected information on patients with tibial fracture between January 2013 and July 2023, and divided them into ACS and non-ACS groups. Propensity score matching (PSM) analysis was performed to lower the impact of potential confounding variables such as demographics and comorbidities. Admission blood indicators were analyzed using univariate, logistic regression, and receiver operating characteristic (ROC) curve analyses. Then, we established a nomogram prediction model by using R language software.ResultsAfter propensity PSM analysis, 127 patients were included in each group. Although numerous blood indicators were found to be relevant to ACS on univariate analysis, logistic regression analysis showed that monocytes (MON, p = 0.015), systemic immune-inflammation index (SII, p = 0.011), and creatine kinase myocardial band (CKMB, p < 0.0001) were risk factors for ACS. Furthermore, ROC curve analysis identified 0.79 × 109/L, 1082.55, and 20.99 U/L as the cut-off values to differentiate ACS patients from patients with tibial fracture. We also found that this combination had the highest diagnostic accuracy. Then, we constructed a nomogram prediction model with AUC of 0.869 for the prediction model, with good consistency in the correction curve and good clinical practicality by decision curve analysis.ConclusionsWe found that the levels of MON, SII, and CKMB were related to ACS and may be potential biomarkers. We also identified their cut-off values to separate patients with ACS from those with tibial fracture, helping orthopedists promptly evaluate and take early measures. We established a nomogram prediction model that can efficiently predict ACS in patients with tibial fracture.

Oleoylethanolamide mitigates cardiometabolic disruption secondary to obesity induced by high-fat diet in mice

Chronic lipid overnutrition has been demonstrated to promote cardiac dysfunction resulting from metabolic derangement, inflammation, and fibrosis. Oleoylethanolamide (OEA), an endogenous peroxisome proliferator activating receptor (PPAR)-α agonist, has been extensively studied for its metabolic properties.The aim of this study was to determine if OEA has beneficial effects on high-fat diet (HFD)-induced cardiac disruption in obese mice, focusing on the underlying pathological mechanisms.OEA treatment restores the metabolic pattern, improving serum glycaemic and lipid profile. OEA also reduces heart weight and serum creatine kinase-myocardial band (CK-MB), a marker of cardiac damage. Accordingly, OEA modulates cardiac metabolism, increasing insulin signaling and reducing lipid accumulation. OEA increases AMPK and AKT phosphorylation, converging in the rise of AS160 activation and glucose transporter (GLUT)4 protein level. Moreover, OEA reduces the transcription of the cardiac fatty acid transporter CD36 and fatty acid synthase and increases PPAR-α mRNA levels. Adiponectin and meteorite-like protein transcription levels were significantly reduced by OEA in HFD mice, as well as those of inflammatory cytokines and pro-fibrotic markers. An increased autophagic process was also shown, contributing to OEA's cardioprotective effects. Metabolomic analyses of cardiac tissue revealed the modulation of different lipids, including triglycerides, glycerophospholipids and sphingomyelins by OEA treatment. In vitro experiments on HL-1 cardiomyocytes showed OEA's capability in reducing inflammation and fibrosis following palmitate challenge, demonstrating a direct activity of OEA on cardiac cells, mainly mediated by PPAR-α activation.Our results indicate OEA as a potential therapeutic to restrain cardiac damage associated with metabolic disorders.

Mortality predictors in acute myocardial infarction: results from a single-center study in Saudi Arabia.

Acute myocardial infarction (AMI) is a leading cause of morbidity and mortality worldwide. Risk factors of mortality in patients with AMI have been widely investigated, identifying older age and heart failure as common contributors. This study aimed to determine risk factors and explore predictors associated with higher mortality among patients with AMI. A retrospective study was conducted at a cardiac center in western Saudi Arabia (KSA) between January 1, 2023, and September 1, 2023. Inclusion criteria comprised patients with a confirmed diagnosis of AMI. Exclusion criteria included patients younger than 18 and those with incomplete diagnostic or follow-up data. A data collection form was generated, including all possible factors associated with mortality among patients with AMI. The study included 851 MI patients with a mean age of 58.78 years, primarily male participants. Survival analysis based on the days of hospitalization revealed that 30-day and 60-day survival rates post-hospitalization were 66.8% and 33.4%, respectively. Patients with acute MI of the anterior wall or other specific sites demonstrated significantly higher risks of mortality compared to those with unspecified acute MI. Elevated creatine kinase-myocardial band (CK-MB) levels and blood urea nitrogen (BUN) were also significantly associated with increased mortality risk. The findings highlighted an association between mortality and diabetes mellitus (DM) and transmural MI of the anterior wall. Significant differences between surviving and deceased patients were observed in several factors, including troponin, CK-MB, low-density lipoprotein (LDL), BUN, creatinine levels, age, and hospital stay duration.

Evaluating the Impact and Financial Implications of Immediate versus Delayed Stenting Strategies in High Thrombus Burden Acute Myocardial Infarction: A Propensity Score-Matched Analysis.

The efficacy of delayed stenting strategies in the management of high thrombus burden acute myocardial infarction remains uncertain. We aimed to compare the therapeutic effects and financial implications of immediate and delayed stenting strategies in patients with acute myocardial infarction and high thrombus burden treated at our institution. This was a retrospective analysis of 158 patients who underwent intracoronary thrombus aspiration for acute ST-elevation myocardial infarction (STEMI) at the Second Affiliated Hospital of Shantou University Medical College between 2013 and 2023. Patients were divided into two groups: immediate stenting (immediate group; n = 101) and delayed stenting (delayed group; n = 57), based on the timing of the stenting procedure. Propensity score matching was performed to minimize confounding bias. Therapeutic effects and cost of treatment were compared between the two groups. After propensity score matching (n = 52 for each group), there were no significant differences in terms of baseline clinical characteristics, characteristics of vascular lesions (number of diseased vessels, culprit vessels, thrombolysis in myocardial infarction (TIMI) thrombus grade, proximal coronary artery lesion), the incidence of no-reflow/slow flow during the first surgery, or the use of antiplatelet drugs, intraprocedural anticoagulants, intracoronary drugs, and tirofiban. There were no significant between-group differences in terms of in-hospital all-cause mortality, in-hospital major adverse cardiovascular events, or hospitalization costs. However, peak creatine kinase-myocardial band (CK-MB) levels were significantly lower in the delayed group. For patients with STEMI undergoing emergency thrombus aspiration, a delayed stenting strategy appears to be non-inferior to immediate stenting strategy in terms of clinical efficacy and hospitalization costs, and may reduce the extent of myocardial injury. Delayed stenting strategy may allow for a more individualized surgical approach based on assessment of thrombus burden and lesion complexity.

Evaluation of protective potency of coconut oil-based probiotic against antibiotic-induced compromised gastrointestinal attributes and associated complications in Swiss albino mice

Background: Antibiotic-induced gastrointestinal toxicity is a major concern globally. The gut-organ axis has been explicitly studied, and hence, any damage to the gut ecosystem directly or indirectly manifests into compromised multi-organ functions. Therefore, the present study was designed to explore the protective potency of coconut oil-probiotic (C-PRO) against antibiotic-induced compromised gastrointestinal attributes and associated complications. Methods: Animals were divided into 5 groups (n=6). Normal saline was given to the control group; the antibiotic cocktail was given to the antibiotic group. In the treatment group, low and high doses of C-PRO were given post-antibiotic treatment. In the per se group, only a high dose of C-PRO was given. After 28 days, animals were studied for neurobehavioral parameters and scarified. Blood and organs were collected and stored for histopathological, immune histochemical, and biochemical analysis. Results: Antibiotic treatment reduced body weight, increased oxidative stress, and caused histopathological damage to the stomach, duodenum, colon, brain, heart, liver, lungs, kidney, spleen, and testis. It also altered biochemical parameters such as lactate dehydrogenase (LDH), creatine kinase-myocardial band (CK-MB), alanine transaminase (ALT), aspartate transaminase (AST), gamma-glutamyl transferase (GGT), albumin, creatinine, urea, uric acid, and blood urea nitrogen (BUN). Additionally, Antibiotic exposure in mice exhibited depressive-like behaviour and declined cognitive function. The treatment with a low dose of C-PROs showed negligible protective effect, whereas a high dose of C-PRO effectively reversed the structural, biochemical, and neurobehavioral attributes toward normal. Conclusions: We conclude that the synergistic effect of coconut oil and probiotics, which have potent antioxidant and anti-inflammatory effects, might be responsible for multidimensional protective effects against compromised gastrointestinal attributes and associated complications.

Nigella sativa oil attenuates inflammation and oxidative stress in experimental myocardial infarction.

A growing interest in using Nigella sativa oil (NSO) in the prevention or treatment of several cardiovascular diseases has prompted this study. The research aims to investigate the effect of NSO on cardiac damage prevention after long-term administration in induced myocardial infarction (MI) in rats. NSO was analyzed for its fatty acids composition using gas chromatography-mass spectrometry (GC-MS) analysis and administered in rats before and after isoproterenol (45mg/kg body weight) induced myocardial infarction. The following parameters were assessed: electrocardiograms, histopathological examination, serum biochemical aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatine kinase-myocardial band (CK-MB), serum and heart inflammation (tumor necrosis factor-alpha (TNF), interleukin 1 beta (IL-1b), and interleukin 6 (IL-6)), and tissue oxidative stress (total antioxidant capacity (TAC), total oxidative stress (TOS), nitric oxide (NO), malondialdehyde (MDA), and the total thiols (THIOL)). Linoleic acid (C18:2n-6) and oleic acid (C18:1n-9) were approximately 89% of total fatty acids while palmitic acid (C16:0) was 6.10%. Administration of NSO for 28 days helped in preventing QT and QTc interval prolongation and reduced heart rate (HR), after MI induction. The histological assessment showed improvement in myofibrillary degeneration and necrosis and also better reduced inflammatory process in the groups treated with NSO. In serum, pro-inflammatory cytokines IL-1b and IL-6 were downregulated in chronic conditions (for IL-1b, NSO vs. control was 86.09vs 150.39 pg/mL, and for IL-6 NSO vs. control was 78.00 vs. 184.98 pg/ml). In the heart tissue, the downregulation was observed only for TNF in both acute and chronic conditions (acute NSO vs. control was 132.37 vs. 207.63 pg/mL, and chronic NSO vs. control was 135.83 vs. 183.29 pg/ml). The pro-oxidant parameters TOS, NO, MDA, and OSI, were reduced in the groups treated with NSO only after 14 days of treatment, suggesting that the NSO antioxidant effect is time-dependent. NSO administration might have a favourable impact on the regulation of oxidative stress and inflammation processes after MI induction in rats, and it is worth considering its administration as an adjuvant treatment.

Clinical Findings, Laboratory Results, Electrocardiography and Echocardiography Findings in Dairy Buffaloes with Theileriosis.

Tropical theileriosis is a tick-borne haemoprotozoan disease, and cardiac function assessment in buffaloes with theileriosis was poorly documented. The Present study was carried out from April 2022 to December 2022. Theileriosis was confirmed by microscopic examination of stained blood smears and lymphnode smearsfurther confirmed by PCR assay. Electrocardiography was performed byusing the base apex lead system, and echocardiography was performed byusing the right parasternal view. The incidence of theileriosis was 16.25% by examination of stained blood smears, and 30.42% by PCR examination in 240 buffaloes. Repeatedly noted clinical signs were the absence of rumination, anorexia, loss of milk yield, depressed demeanour, emaciation, hyperthermia, lymphadenopathy, tick infestation, tachycardia, cardiac arrhythmia, and increased intensity of heartbeat. Haematological findings disclosed decreased haemoglobin, packed cell volume, total erythrocyte count, and neutrophils; increased eosinophils and monocytes. Serum biochemical findings revealed decreased albumin, albumin/globulin ratio, glucose, calcium, phosphorous, sodium, potassium, and chloride; increased globulin, aspartate aminotransferase, bilirubin, blood urea nitrogen, creatinine, cholesterol, lactate dehydrogenase, gamma-glutamyl transferase, and creatine kinase myocardial band isoenzymes. Electrocardiography explorations were sinus tachycardia, broad T wave, and sinus arrhythmia. Echocardiography examination showed ventricular wall thickening, cardiac chamber dilatation, valvular defects/valvular regurgitation, and pericarditis/cardiac tamponade. The present research proposes the changes in the electrocardiography and echocardiography findings in buffaloes with theileriosis, which are essential in clinics to identify the secondary complications during theileriosis and formulate therapeutics.

Acute cardiorenal dysfunctions induced by isoprenaline in Wistar rats: Mitigating potential of Juglans regia hull extract

The present study aimed to determine the attenuating properties of Juglans regia hull extract (JRHE) in mitigating isoprenaline (ISO) induced cardiorenal dysfunctions in Wistar rats. Thirty adult Wistar rats were randomly allocated to five groups with six animals in each group. Group I served as control; group II animals were administered ISO and group III received JRHE alone whereas group IV and V received JRHE and quercetin along with ISO, respectively. Administration of ISO in rats induced cardiac and renal tissue damage as reflected by significantly (p < 0.05) increased plasma activities of creatine kinase-myocardial band, lactate dehydrogenase, acetylcholinesterase, arylesterase, blood urea nitrogen, creatinine along with altered antioxidant biomarkers viz. total antioxidant status, total thiols, superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase and increased (p < 0.05) lipid and protein peroxidation in cardiac and renal tissues. Histopathological findings corroborated that ISO has inflicted significant damage on cardiac and renal tissues. Repeated administration of JRHE significantly (p < 0.05) reduced the severity of ISO-induced alterations in blood, cardiac and renal biomarkers. In addition to restoring the levels of altered cardio-renal antioxidant enzymes, JRHE also ameliorated histopathological lesions in cardiac and renal tissues in ISO-treated rats.

Cardioprotective Efficacy of Sevoflurane in Patients With Rheumatic Heart Disease Undergoing Heart Valve Surgery Under Cardiopulmonary Bypass.

In this study, we investigated whether cardioprotective properties of sevoflurane were expressed in patients with rheumatic heart disease undergoing heart valve surgery under cardiopulmonary bypass (CPB). Fifty patients with rheumatic heart disease undergoing heart valve surgery under CPB were randomly assigned to receive total anesthesia with sevoflurane or propofol during surgery. Except for this, anesthetic and surgical management was the same in all patients. The primary outcomes were postoperative high-sensitive cardiac troponin T (hs-cTnT) and creatine kinase-myocardial band (CK-MB) release. The secondary outcomes were hemodynamic events and short-term clinical outcomes (within 30 days after surgery). The plasma concentrations of hs-cTnT at 24-hour and CK-MB from 6-hour to 48-hour in the sevoflurane group were lower than those in the control group (the propofol group). After aortic unclamping, heartbeat recovery was faster and the rate of sinus rhythm was higher in the sevoflurane group than in the control group. Moreover, a lower proportion of pacemaker use and the need for intraoperative and postoperative inotropes were also found in the sevoflurane group. Nevertheless, there were no differences between the two groups regarding short-term clinical outcomes (durations of mechanical ventilation, intensive care unit stay, hospital stay, morbidity, and mortality rates). Sevoflurane administered during the entire anesthetic procedure had a myocardial protective effect with less evidence of myocardial damage in the first 48-hour postoperatively but short-term clinical outcomes were not significantly different when compared with the control group in patients with rheumatic heart disease undergoing heart valve surgery under CPB.

Cardioprotective effect of chelidonic acid against doxorubicin-induced cardiac toxicity in rats

Introduction and objectivesThe current study evaluates the effect of chelidonic acid on doxorubicin-induced cardiac toxicity. Chelidonic acid (CA) is a natural pyran-skeleton heterocyclic compound found in rhizomes of the perennial plant, celandine (Chelidonium majus). MethodsWistar rats were given an intraperitoneal injection of doxorubicin (1.25 mg/kg, cumulative dose of 20 mg/kg) four times per week for a duration of four weeks to induce cardiotoxicity. CA treatment (10, 20, and 40 mg/kg orally for four weeks) was started together with doxorubicin. ResultsCA treatment reduced myocardial damage and improved cardiac dysfunction in doxorubicin-treated rats. It improved blood pressure, restored ST wave height and normalized the QTc interval compared to the rats treated only with doxorubicin. Administration of CA for four weeks reduced left ventricular end-diastolic pressure. Moreover, CA treatment decreased the level of cardiac markers such as creatine kinase-myocardial band (CK-MB), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), and cardiac troponin-T. Masson's trichrome, hematoxylin, and eosin staining of heart tissue revealed that CA attenuated the deleterious effects of doxorubicin and prevented further damage and fibrosis in rats. ConclusionThe study findings confirm that CA treatment can protect the myocardium against doxorubicin-induced cardiotoxicity.

The effects of berberine and curcumin on cardiac, lipid profile and fibrosis markers in cyclophosphamide-induced cardiac damage: The role of the TRPM2 channel.

Cyclophosphamide (CYP) is widely used to treat various types of cancer. In addition to the therapeutic properties of this drug, unfortunately, its side effects are still not fully understood. This study investigated the protective effect of curcumin (CURC) and berberine (BER) on CYP-induced cardiac damage. Thirty-six male rats were equally divided into the control, dimethyl sulfoxide (DMSO), CYP, CYP + CURC, CYP + BER and CYP + BER + CURC groups. Troponin-I, Creatine kinase-myocardial band (CK-MB), total cholesterol, triglyceride levels in serum samples, and reactive oxygen species (ROS), poly(ADP-ribose) polymerase-1 (PARP-1), and transient receptor potential melastatin 2 (TRPM2) channel levels in heart tissue were measured using an enzyme-linked immunoassay (ELISA) kit. In addition, histopathological examination and immunohistochemical investigation of the TRPM2 channel, fibroblast specific protein-1 (FSP1), transforming growth factor-beta- 1 (TGF-β1) and α-smooth muscle actin (α-SMA) expressions were determined in heart tissue. The CYP group's troponin-I, total cholesterol, triglyceride, CK-MB, ROS, PARP-1 and TRPM2 channel levels were higher than in the other groups in the ELISA measurements (p < 0.05). In contrast, these parameters in the group treated with CURC and BER together with CYP were lower than in the CYP group (p < 0.05). Additionally, CUR and BER reduced CYP-induced pathological damage, TRPM2, FSP1, TGF-β1 and α-SMA expressions. The data showed that CYP administration can cause cardiac damage by increasing the TRPM2 channel, TGF-β1, FSP1 and α-SMA expression levels. Therefore, we concluded that CURC and BER administration following CYP application may be used as therapeutic agents to prevent CYP-induced cardiac damage.