Creatine Kinase Isoenzyme MB Activity Research Articles

Effect of dapagliflozin on blood glucose control, cardiac function, and myocardial injury markers in patients with type 2 diabetes and heart failure

Purpose: To investigate the impact of dapagliflozin treatment on blood glucose control, cardiac function, and myocardial injury markers in patients with type 2 diabetes and heart failure. 
 Methods: In a retrospective analysis of clinical data for 132 patients with type 2 diabetes and heart failure admitted to Beijing Tongren Hospital, China from January 2020 to June 2021, these patients were stratified into two groups (66 patients each). Control group received conventional pharmacotherapy and study group received additional treatment with dapagliflozin. Both treatment courses lasted for 6 months. The levels of blood glucose control, cardiac function, and myocardial injury markers before and after 6 months of treatment were compared between the two groups, as well as safety during treatment. 
 Results: After 6 months of treatment, both groups exhibited significant reductions in fasting plasma glucose (FPG), 2-h postprandial glucose (2 h PG), glycated hemoglobin (HbA1c), N-terminal pro-brain natriuretic peptide (NT-proBNP), cardiac troponin I (cTnI), creatine kinase-MB isoenzyme activity (CK-MB), aspartate aminotransferase (AST) levels, left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), and Minnesota Living with Heart Failure Questionnaire (MLHFQ) score, with study group showing a greater improvement (p < 0.05). 
 Conclusion: Dapagliflozin enhances blood glucose control and cardiac function, improving quality of life in patients with type 2 diabetes and heart failure. Furthermore, Dapagliflozin demonstrates a safe and well-tolerated profile. Future studies will require establishing the mechanism of dapagliflozin action in a larger and more diverse population.

Selenium mitigated aflatoxin B1-induced cardiotoxicity with potential regulation of 4 selenoproteins and ferroptosis signaling in chicks

The aim of the present study was to explore the underlying mechanism of selenium (Se)-mediated detoxification of aflatoxin B1 (AFB1)-induced cardiotoxicity in chicks. A Se-deficient, corn-soybean meal-basal diet (36 μg Se/kg, BD) and three test diets (BD+1.0 mg AFB1/kg, 0.3 mg Se/kg, or 1.0 mg AFB1/kg+0.3 mg Se/kg) were used in a 3-wk 2 × 2 factorial design trial (n = 30 chicks/group). Dietary AFB1 led to induced (P < 0.05) serum creatine kinase and creatine kinase MB isoenzyme activities and heart histopathologic lesions. However, Se deficiency aggravated most of these alterations induced by AFB1. Moreover, mRNA levels of two ferroptosis activators (solute carrier family 11 Member 2 and transferrin) were upregulated (P < 0.05) in the AFB1-treated groups. Additionally, Se deficiency reduced (P < 0.05) glutathione peroxidase (GPX) 3 and thioredoxin reductase 3 mRNA and GPX activity but increased (P < 0.05) selenoprotein M and selenophosphate synthetase 2 mRNA in the heart in AFB1-administered groups. The in vitro study showed that Se alleviated (P < 0.05) AFB1-reduced cell viability and induced (P < 0.05) ROS and ferroptosis in H9C2 cardiac cells. It also downregulated (P < 0.05) two ferroptosis activators (long-chain acyl-CoA synthetase 4 and solute carrier family 11 Member 2) in the AFB1-treated groups in the H9C2 cells. In conclusion, this study illustrated that Se alleviates AFB1-induced cardiotoxicity and cardiomyocyte damage potentially related to the regulation of redox status, 4 selenoproteins, and ferroptosis-related signaling.

Comprehensive non-invasive assessment of electrocardiographic abnormalities and cardiac arrhythmias in patients with genetically confirmed mitochondrial diseases

BackgroundThere is limited data on cardiac arrhythmias and ventricular repolarization and dispersion abnormalities in patients with mitochondrial diseases (MitD). MethodsConsecutive 40 patients with genetically proven MitD and 35 healthy controls were studied. Among other examinations all subjects underwent 24-h Holter recording and 12‑lead electrocardiography (ECG) with corrected QT (QTc), QT dispersion (QTd), Tp-e and Tp-e/QT ratio assessment. ResultsPatients with MitD were 55.4 ± 15.7 years old, the disease duration was 18.5 ± 10.3 years, presented 6 clinical syndromes while mitochondrial and nuclear DNA type of mutation was present in 40 and 60% of cases, respectively. In MitD more frequently 1st degree atrioventricular block and intraventricular conduction defects were observed and also QRS complex duration was increased. Mean values of QTc (p = 0.001), QTd (p = 0.02), Tp-e (p < 0.00001) and Tp-e/QT (p < 0.00001) were significantly higher in MitD than in controls. Correlations between disease duration and PR interval duration (p = 0.003) and Creatine Kinase MB isoenzyme activity (p = 0.02) were found. No differences in depolarization and dispersion parameters were observed according to type of mutation or dominant clinical syndromes. In addition to supraventricular extrasystoles, nonsustained supraventricular tachycardias occurred more frequently in MitD (in 45.0 vs 14.3%, p = 0.0004). Ventricular arrhythmias were rare and observed almost exclusively in subjects with mitochondrial DNA mutation. ConclusionsIn contrast to healthy controls, in MitD patients intraventricular, repolarization and dispersion disturbances were more frequently observed. In addition to bradyarrhythmias observed in some defined MitD syndromes, supraventricular rather than ventricular arrhythmias are more common.

Misoprostol ameliorates doxorubicin induced cardiac damage by decreasing oxidative stress and apoptosis in rats

ABSTRACT We investigated the potential cardioprotective effects of misoprostol (MP) on doxorubicin (DOX) induced cardiac damage using histologic and biochemical assessment of rat heart. We used 21 male rats divided randomly into three groups: group 1, control; group 2, DOX; group 3, DOX + MP. The control group was given 0.5 ml 0.9% NaCl intraperitoneally (i.p.) and 1 ml 0.9% NaCl orally for 6 days. DOX was administered as a single dose of 20 mg/kg i.p. on day 3. MP was administered orally for 6 days. We found that treatment with MP decreased significantly serum cardiac troponin-I, brain natriuretic peptide levels, and lactate dehydrogenase, aspartate aminotransferase, alanine transaminase and creatine kinase isoenzyme-MB activities. DOX increased the malondialdehyde level and decreased the catalase, superoxide dismutase activities and glutathione levels; MP prevented these alterations. MP also decreased NADPH oxidase-4 and caspase-3 levels. In the DOX + MP group, oxidative stress was decreased, antioxidant activity was increased and histopathological changes were decreased compared to the DOX group. Cardiac damage caused by DOX was attenuated by MP treatment owing to the antioxidative and anti-apoptotic effects of MP. MP may be useful for reducing the severity of DOX induced damage.

Protective effect of N-acetyl cysteine against radiotherapy-induced cardiac damage

Purpose: Although radiotherapy (RT) is an important component of cancer treatment, it induces adverse tissue reactions in the around of cancer tissue. Therefore, radioprotectives are needed to protect normal tissues. The aim of this study was to investigate the radioprotective effect of N-acetylcysteine (NAC) on RT-induced cardiac damage in rats for the acute term.Materials and methods: The animals were divided into four groups. The rats in control group were injected with saline for 7 d; the rats in NAC group were injected NAC at dose of 240 mg/kg d for 7 d; the rats in RT group were injected with saline for 7 d plus was irradiated 1 h after the last injection and the rats in NAC + RT group were injected with NAC for 7 d and irradiated 1 h after the last NAC dose. The electrocardiogram was recorded and evaluated PR interval, QRS duration, QT interval, T wave alterations and heart rate. Serum interleukin-4, interleukin-6, tumor necrosis factor-alpha, interleukin 1 beta, galectin-3 levels and creatine kinase and creatine kinase isoenzyme-MB activities were determined in all groups. Also, tissue malondialdehyde (MDA) and nitric oxide levels, superoxide dismutase, catalase and glutathione peroxidase activities were determined. In addition, histological changes of heart were evaluated. All measurements were performed 24 h after RT.Results: In the RT group, findings supporting cardiac injury were observed in the electrocardiogram. Also, cytokine levels and oxidative stress were significantly increased. Pretreatment of rats with NAC ameliorated cardiac injury induced by RT.Conclusions: Our findings suggested that NAC may be a potential radioprotector which is capable of preventing cardiac damage.

Differential IL 10 serum production between an arm-based and a leg-based maximal resistance test

Bench press (i.e. arm-based) and half-squat (i.e. leg-based) are exercises commonly used to increase and evaluate muscular strength. In addition to differences in the location of the muscles that participate in each exercise, the total muscle mass required for the latter is larger than that involved in the former. The aim of this study is to analyze the effects of a maximal incremental strength test when performed by bench press and by half-squat on myocellular damage, oxidative damage and the inflammatory cytokine response. Ten male athletes were subjected to half-squat and bench press incremental strength tests. Blood samples were collected at rest, 15-minutes and 24 h post-test. Hydroperoxide and malondialdehyde concentrations were determined as lipid peroxidation markers. Lactate dehydrogenase (LDH) and creatine kinase isoenzyme MB (CK-MB) activities were determined as markers of muscle damage. α-Actin concentration was determined as a marker of sarcomeric damage. Serum interleukin (IL) 6, IL10, and tumor necrosis factor alpha (TNFα) were determined to assess the inflammatory response. LDH and CK-MB values were greater at 15 min and 24 h post bench press exercise (p < 0.05). No differences were found in lipid peroxidation or α-actin. Interestingly, IL10 values were greater in response to the press bench at 24 h post-test (p < 0.05). Our results suggest that, at equivalent workloads, an arm-based exercise induced higher anti-inflammatory effects and more severe muscle damage compared with a leg-based exercise.

Protective effect of supplementation with Lycium ruthenicum Murray extract from exhaustive exercise-induced cardiac injury in rats.

To the Editor: Lycium ruthenicum (L. ruthenicum) Murray contains abundant anthocyanins. The purpose of the present research was to investigate the protective effect of L. ruthenicum extract supplementation on the damage from exhaustive exercise in rats which were treated for seven days before the exhaustive exercise. Exhaustive exercise induced an increase of Serum nitrate (NO) and reactive oxygen species (ROS) levels, but supplementation of L. ruthenicum extract reduced them significantly (P < 0.05). Interleukin (IL)-1 and IL-6 were also significantly reduced by L. ruthenicum as compared to the control (P < 0.05). Supplementation with L. ruthenicum extract also decreased the creatine kinase isoenzyme MB (CK-MB) generation significantly and ameliorated the myocardial histopathology. L. ruthenicum belongs to the genus Lycium of the family Solanaceae and is a salinized desert plant distributed mainly in Qinghai and Xinjiang Provinces of China. Recently, studies have shown that L. ruthenicum exhibits a wide range of pharmacologic properties, such as anti-oxidation, anti-fatigue, and hypoglycemic activity.[1,2] Anthocyanins and their aglycones from L. ruthenicum have strong antioxidant activity.[3] Anthocyans are flavonols, which occur ubiquitously in the plant kingdom and confer bright red or blue coloration on berries and other fruits and vegetables. Anthocyanin concentration in the L. ruthenicum extract was determined by using the Nakata method[4] and the concentration in the L. ruthenicum extract was 24.1 ± 7.7 mg/g. However, we know anthocyanin has antioxidant properties and ROS induced by extreme temperatures can be protected by anthocyanins in several plants. Anthocyanin has an antioxidant role in plants against ROS and extreme temperatures. Exercise-induced oxidative stress has been reported and antioxidant supplementation can prevent muscle damage, protective effects on the endocrine-metabolic and immune profile.[5] Therefore, L. ruthenicum extract should have a protective effect against oxidative stress and we investigated that the possible protective effect of L. ruthenicum extract and anthocyanin supplementation on the oxidative stress generated by exhaustive exercise in SD rats. In this study, 30 Sprague-Dawley (SD) rats, males and aged 6 weeks, were randomly assigned to the control, anthocyanin (5 mg/rat as the positive control), and other three groups were given L. ruthenicum extract in distilled water orally (as vehicle, 10 and 30 mg/rat), for 7 days before the exhaustive exercise stress. Rats of the exhaustive exercise group were subjected to graded treadmill running started at 10% grade, 15 m/min for 10 min followed by gradual increases of treadmill speed and time as 25 m/min for 20 min, 28 m/min for 20 min, 31 m/min for 20 min, 34 m/min for 20 min, 37 m/min for 20 min until exhaustion. The heart was dissected and washed with saline for fixation with formalin. Exhaustive exercise causes oxidative stress and is defined as the inability of rats to run on the treadmill despite a mild electrical shocking.[6] Add some information on dietary antioxidants for exercise-induced oxidative stress.[7] Regular exercise is recommended for a healthy life, but exhaustive exercise generates the excessive oxidative stress that may exceed the beneficial effect from the regular exercise.[8] In the present study, an increasing CK-MB activity from the cardiac muscle consisted of myocardial damage was seen in tissue vacuoles and cell death from heart tissue. Exhaustive exercise also induced an increase of serum NO, ROS, IL-1, IL-6, and CK-MB levels, but supplementation of L. ruthenicum extract reduced them significantly. Supplementation with L. ruthenicum extract also significantly ameliorated the myocardial histopathology. Under the microscope, the photographs showed the heart section with a 400× magnification. The severity of damage in the exhaustive exercise group was exhibited by vacuoles and dead cells. However, changes in histopathology were significantly reduced by the treatment with anthocyanin and L. ruthenicum extract [Figure 1].Figure 1: Protective effect of Lycium ruthenicum extract on the exhaustive exercise-induced myocardial injury. Histopathology (hematoxylin and eosin staining) of myocardial slices from rats from (A) no treatment control group; (B) the exhaustion group; (C) the Anthocyanin group, exhaustive exercise treatment supplemented with 5 mg Anthocyanin/rat; and (D) the L. ruthenicum extract group, exhaustive exercise treatment supplemented with 30 mg L. ruthenicum/rat. Photographs show the myocardial section with 400× magnification. Tissue vacuoles (hollow triangle arrow heads ▿) and cell death (nuclei stained, black arrow heads ◂) were more severe in exhaustion than those in control or L. ruthenicum groups.In conclusion, 1-week oral supplementation of L. ruthenicum extracts present positive effects on the oxidative stress generated by exhaustive exercise in SD rats, possibly via promotion of antioxidant capacity. The mechanism of protection of L. ruthenicum extract supplementation was not investigated in this study and waits for further study in the future. Acknowledgements The authors are grateful for text proofreading support from Prof. Kee-Ching Jen. Funding None. Conflicts of interest None.

Prognostic Value of Serum Troponin T in Unstable Angina.

Abstract Background. Cardiac troponin T is a regulatory contractile protein not normally found in blood. Its detection in the circulation has been shown to be a sensitive and specific marker for myocardial cell damage. We used a newly developed enzyme immunoassay for troponin T to determine whether its presence in the serum of patients with unstable angina was a prognostic indicator. Methods. We screened 109 patients with unstable angina (25 with accelerated or subacute angina and 84 with acute angina at rest) for serum creatine kinase activity, creatine kinase isoenzyme MB activity, and troponin T every eight hours for two days after admission to the hospital. The outcomes of interest during the hospitalization were death and myocardial infarction. Results. Troponin T was detected (range, 0.20 to 3.64 μg per liter; mean, 0.78; median, 0.50) in the serum of 33 of the 84 patients (39 percent) with acute angina at rest. Only three of these patients had elevated creatine kinase MB activity (two were positive...

Changes in heart rate, arrhythmia frequency, and cardiac biomarker values in horses during recovery after a long-distance endurance ride.

OBJECTIVE To evaluate heart rate, heart rate variability, and arrhythmia frequency as well as changes in cardiac biomarker values and their association with heart rate in horses before and after an endurance ride. DESIGN Cross-sectional study. ANIMALS 28 Arabian horses competing in a 120- or 160-km endurance ride. PROCEDURES ECG recordings were obtained from each horse before (preride) and after (recovery) an endurance ride to evaluate changes in heart rate and the SD of normal R-R intervals (SDNN) during the initial 12 hours of recovery. Frequencies of supraventricular and ventricular premature complexes before and after the ride were evaluated. Blood samples were obtained before the ride and twice during recovery. Hematologic analyses included measurement of serum cardiac troponin I concentration and creatine kinase isoenzyme MB activity. RESULTS Heart rate was significantly increased and SDNN was decreased during the recovery versus preride period. Frequency of ventricular premature complexes increased during recovery, albeit not significantly, whereas frequency of supraventricular premature complexes was not significantly different between preride and recovery periods. Serum cardiac troponin I concentration and creatine kinase isoenzyme MB activity were significantly increased in the recovery versus preride period. No associations were identified between cardiac biomarkers and velocity, distance, or mean heart rate. CONCLUSIONS AND CLINICAL RELEVANCE Heart rate increased and SDNN decreased in horses after completion of an endurance ride. These and other cardiac changes suggested that prolonged exercise such as endurance riding might have cardiac effects in horses. Additional studies are needed to clarify the clinical relevance of the findings.

Effect of high-level spinal cord injury on myocardial energy metabolism in rats

Objective To evaluate the effect of high-level spinal cord injury (SCI) on the myocardial energy metabolism in rats. Methods Sixty healthy male Sprague-Dawley rats, weighing 250-300 g, were randomly divided into 2 groups (n=30 each) using a random number table: sham operation (group S) and SCI group. SCI was induced in anesthetized rats by dropping a 10 g weight onto C7 spinal cord from 5 cm height falling freely inside a vertical hollow glass tube. At 6, 12, 24, 48 and 72 h after SCI, 6 rats in each group were chosen and arterial blood samples were taken for measurement of serum creatine kinase (CK) and creatine kinase isoenzyme-MB (CK-MB) activities. The rats were then sacrificed and myocardial specimens were obtained for examination of myocardial ultrastructure and for determination of ATP weight ratio, levels of Na+-K+-ATPase, Ca2+-Mg2+-ATPase, non-esterified fatty acids (NEFA) and lactic acid (LD), and expression of peroxisome proliferator-activated receptor alpha (PPARα) mRNA and protein (using fluorescent quantitative PCR and Western blot). Results Compared with group S, the serum CK and CK-MB activities were significantly increased, the ATP weight ratio, activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase and levels of NEFA and LD were decreased, and the expression of PPAR-α mRNA and protein was down-regulated in SCI group. No pathological changes of myocardium were found in group S, and the pathological changes of myocardium were obvious in SCI group. Conclusion High-level SCI can lead to decrease in the myocardial energy metabolism in rats, and down-regulated expression of PPARα is involved in the mechanism. Key words: Spinal cord injuries; Myocardium; Energy Metabolism; Peroxisome proliferators

Effects of pretreatment with nerve growth factor-beta on ischemia-reperfusion injury in isolated rat hearts:a comparison with preconditioning

Objective To evaluate the effect of pretreatment with nerve growth factor-beta (NGF-β) on ischemia-reperfusion (I/R) injury in isolated rat hearts by comparing it with NGF-β preconditioning.Methods Pathogen-free male Sprague-Dawley rats,weighing 200-300 g,aged 8-10 weeks,were anesthetized with intraperitoneal 10％ chloral hydrate 300 mg/kg.Their hearts were excised and perfused in a Langendorff apparatus with KH solution aerated with 95％ O2 and 5％ CO2 at 37℃.Twenty-four isolated rat hearts were randomly divided into 3 groups (n =8 each) using a random number table:I/R group,NGF-β pretreatment group (group NGFPt) and NGF-β preconditioning group (group NGFPc).The hearts were perfused with K-H solution for 10 min (equilibration) in each group.In group I/R,the hearts were continuously perfused with K-H solution for 30 min.The hearts were continuously perfused with K-H solution containing NGF 0.1 μg/ml for 20 min before ischemia in group NGF-Pt.The hearts were continuously perfused with K-H solution containing NGF 0.1 μg/ml for 20 min followed by 10 min washout before ischemia in group NGFPc.The perfusion was suspended for 30 min followed by 120 min of reperfusion with K-H solution in each group.HR,left ventricular end-diastolic pressure (LVEDP),left ventricular developed pressure (LVDP) and + dp/dtmax were measured at the end of 10 min equilibration (baseline,T1),immediately before suspension of perfusion (T2),and at 5,30,60 and 120 min of reperfusion (T3-6).The activities of creatine kinase isoenzyme-MB (CK-MB) and lactate dehydrogenase (LDH) in coronary effluent were measured at T1 and T3-6.Myocardial specimens were obtained at T6 for detection of myocardial apoptosis (by TUNEL) and for microscopic examination.Apoptotic index (AI) was calculated.Results Compared with the baseline value at T1,+ dp/dtmax was significantly decreased,and LVEDP and activities of CK-MB and LDH were increased at T3-6 in each group,LVDP and HR were decreased at T3-6 in group I/R,LVDP was decreased at T3,4 in group NGFPt and at T3-6 in group NGFPc,and HR was increased at T2-6 in NGFPt and NGF Pc groups (P ＜ 0.05).Compared with group I/R,LVDP,+ dp/dtmax and HR were significantly increased and LVEDP and activities of CK-MB and LDH and AI were decreased in NGFPt and NGFPc groups (P ＜ 0.05).Compared with group NGFPc,LVDP,+ dp/dtmax and HR were significantly increased,while the LDH activity and AI were decreased (P ＜ 0.05) and no significant changes were found in LVEDP and CK-MB activity in group NGFPt (P ＞ 0.05).The pathologic changes of myocardium were significantly reduced in NGFPt and NGFPc groups as compared with I/R group.Conclusion Pretreatment with 0.1 μg/ml NGF-β attenuates I/R injury in isloated rat hearts,and the efficacy is superior to that of NGF-β preconditioning. Key words: Nerve growth factor; Ischemic preconditioning; Myocardial reperfusion injury; Pretreatment

Effect of the Inhibition of Mitochondrial Creatine Kinase Activity on the Clinical Diagnosis of Suspected Acute Myocardial Infarction

Background: Creatine kinase isoenzyme MB (CK-MB) activity using the immunoinhibition method has been measured in clinical laboratories. However, the presence of mitochondrial CK (MtCK) abnormally increases CK-MB ac- tivity when measured using the conventional method, which can lead to misdiagnosis of acute myocardial infarction (AMI). A new CK-MB activity assay kit that can inhibit MtCK activity was recently developed; here, we describe the per- formance of this kit. Methods: The analytical performance of this new kit was investigated using 338 samples, and the correlation between re- sults obtained using the new and conventional kits were analyzed. Results: A good correlation (r > 0.993) was found between results obtained using the new and conventional kits in the sera from patients with obvious AMI (n = 91). However, a poor correlation exists between results obtained using the new and conventional kits in samples from patients without AMI. Electrophoretic CK isoenzyme analysis confirmed that the ap- pearance of MtCK in nearly all samples from patients with malignant tumors makes poor correlation. Conclusion: Inhibiting MtCK activity is important for diagnosing AMI. The new method may provide a more accurate value of CK-MB activity for clinical use.

The Optimal Strategy of Noninvasive Limb Ischemic Preconditioning for Protecting Heart Against Ischemia-Reperfusion Injury in Rats

Limb ischemic preconditioning (LIPC) induced by prior brief periods of ischemia-reperfusion (I/R) to a limb is a simple and convenient strategy to protect the heart from I/R injury. However, the optimal strategy is unknown. Therefore, the present study was conducted to test the most effective method of LIPC for clinical applications. Male Wistar rats were randomized into the following groups: control groups, consecutive LIPC groups, intermittent LIPC groups. The control groups, including the sham operation group, the ischemia-reperfusion (I/R)-control group, the myocardial ischemic preconditioning (MIPC) group, the femoral artery ischemic preconditioning (FAIP) group; the consecutive LIPC groups, including continuously using for 1 d, 3 d, and 7 d groups. Each group was tested on the first, third, and fifth d after LIPC; intermittent LIPC groups, including 1-d LIPC + 1-d interval group, 1-d LIPC + 2-d interval group, 3-d LIPC + 3-d interval group, 3-d LIPC + 5-d interval group. Left ventricular function, incidence of ventricular arrhythmia, and ST-segment were measured during I/R. Myocardial infarct size, creatine kinase isoenzyme MB (CK-MB), and cardiac troponins I (cTnI) were determined at the end of experiment. Compared with the I/R-controls, the MIPC, FAIP, continuous LIPC for 3 and 7 d and 1-d LIPC + 1-d interval groups showed amelioration of ventricular arrhythmia, improved left ventricular function, lower ST-segment elevation, reduced myocardial infarct size, decreased CK-MB, and cTnI activity. The protective effects of LIPC persisted for 72 h. Our results suggest that a 1-d LIPC + 1-d interval provides optimal cardioprotection from I/R.

The Effects of Two Different Dosages of BCAA Supplementation on A Serum Indicators of Muscle Damage in Wrestlers

Background and Aim: Few studies have been done to examine the effect of different dosages of branched-chain amino acid (BCAA) supplementation on muscle damage indices in wrestlers. The purpose of this research was to compare the effects of two dosages of BCAA on muscle damage indices after heavy resistance exercise in wrestlers. Methods: 29 young wrestlers were randomly selected and divided into three groups. All subjects participated in heavy weight resistance exercise (3 sets, 10 repetitions, 80% 1RM). The BCAA was given at doses of 210 and 450 mgkg −1 body weight for supplemental groups 1 and 2 respectively, 30 minutes before and after the exercise test and dextrin was given at a dose of 210 mg.kg−1 body weight for the placebo group. To identify enzyme activity (IU/L), venous blood samples were obtained 30 min prior to exercise and at 24 and 48 hrs post exercise. Data were statistically analyzed using ANOVA with repeated measures and the Bonfferoni test (P≥ 0. 05). Results: Based on this study results, creatine kinase (CK), lactate dehydrogenase (LDH), creatine kinase isoenzyme MB (CKMB) activity were significantly increased (p<0.05) in all groups. CK, LDH, CKMB indices having the highest activity in the placebo group, but there were no significant differences between all groups. Conclusion: These results provide evidence that the use of two different dosages of BCAA did not decrease the muscle damage associated with heavy resistance exercise.

In Vivo Cardioprotection by Pitavastatin From Ischemic-reperfusion Injury Through Suppression of IKK/NF-κB and Upregulation of pAkt–e-NOS

Recent studies have uncovered the beneficial effects of statin in cardiovascular diseases; however, the role of pitavastatin in ischemia-reperfusion (IR)-induced apoptosis and myocardial damage is not established. Therefore, in this study, we aim to investigate whether pitavastatin treatment attenuates myocardial IR injury via regulating oxidative stress, inflammation, apoptosis, and phosphorylated protein kinase B (pAkt) endothelial nitric oxide synthase (e-NOS) pathways. After the 14-day treatment with pitavastatin (0.16-0.64 mg·kg·d, po) or saline, rats were subjected to 45 minutes of ischemia by occluding the left anterior descending coronary artery and to 60 minutes of reperfusion to induce myocardial damage. Pitavastatin at a dose of 0.32 and 0.64 mg/kg significantly improved cardiac function as evidenced by the normalization of the mean arterial pressure, heart rate, ±LVdP/dtmax, and left ventricular end-diastolic pressure as compared with the IR control. Additionally, pitavastatin dose-dependently normalized myocardial antioxidants, lactate dehydrogenase, and thiobarbituric acid reactive substances along with decreased serum tumor necrosis factor-α level and creatine kinase isoenzyme-MB activity. Furthermore, pitavastatin enhanced pAkt, (p) e-NOS, Bcl-2, and suppressed IκB kinase/nuclear factor-kappa B, nitrotyrosine (NO inactivation product), Bax, and capases-3 protein expression in the heart. Morphological assessments of the IR-challenged myocardium showed that 0.32 and 0.64 mg/kg of pitavastatin decrease myocardial necrosis and inflammatory changes. Thus, pitavastatin reduced IR-induced infarction and dysfunction via the augmentation of endogenous antioxidant, suppression of IκB kinase/nuclear factor-kappa B, activation of pAkt-e-NOS, and/or decreased NO inactivation and apoptosis.

Development and performance of an enzyme immunoassay to detect creatine kinase isoenzyme MB activity using anti-mitochondrial creatine kinase monoclonal antibodies

Objective: The MB fraction of creatine kinase (CK-MB) has long been used as a cardiac marker. It is known that the CK-MB immunoinhibition method lacks selectivity and accuracy, because the appearance of macro CK type 2, corresponding to mitochondrial creatine kinase (MtCK) in some patient serum may render CK-MB activity measured by conventional method abnormally high. Thus, to improve the specificity and accuracy of the CK-MB assay, we developed two types of monoclonal anti-MtCK antibodies against sarcomeric MtCK and ubiquitous MtCK, and present herein the performance of a new method using these antibodies. Material and methods: The performance of our test for detecting CK-MB activity was compared with other methods, and the range of CK-MB activities in normal human serum was investigated. Results: The two types of monoclonal antibodies developed by us were isoenzyme-specific to sMtCK or uMtCK. The correlation coefficients of our method and conventional method to electrophoresis were 0.973 and 0.873, respectively. The mean CK-MB activity in normal human serum by our method and the conventional method was 2.4 and 11.7 U/L, respectively. Thus, our data indicated that about 80% of CK-MB activity, determined using the conventional method, seems to correspond to the MtCK activity. Conclusion: Our method is novel in offering higher accuracy of measuring true CK-MB contents in human serum as compared to the conventional method. The possibility of accurately estimating CK-MB activity by our method which can inhibit MtCKs in healthy person and patient serum is likely to bring a break-through in clinical diagnostics.

Development and performance of an enzyme immunoassay to detect creatine kinase isoenzyme MB activity using anti-mitochondrial creatine kinase monoclonal antibodies

Objective: The MB fraction of creatine kinase (CK-MB) has long been used as a cardiac marker. It is known that the CK-MB immunoinhibition method lacks selectivity and accuracy, because the appearance of macro CK type 2, corresponding to mitochondrial creatine kinase (MtCK) in some patient serum may render CK-MB activity measured by conventional method abnormally high. Thus, to improve the specificity and accuracy of the CK-MB assay, we developed two types of monoclonal anti-MtCK antibodies against sarcomeric MtCK and ubiquitous MtCK, and present herein the performance of a new method using these antibodies. Material and methods: The performance of our test for detecting CK-MB activity was compared with other methods, and the range of CK-MB activities in normal human serum was investigated. Results: The two types of monoclonal antibodies developed by us were isoenzyme-specific to sMtCK or uMtCK. The correlation coefficients of our method and conventional method to electrophoresis were 0.973 and 0.873, respectively. The mean CK-MB activity in normal human serum by our method and the conventional method was 2.4 and 11.7 U/L, respectively. Thus, our data indicated that about 80% of CK-MB activity, determined using the conventional method, seems to correspond to the MtCK activity. Conclusion: Our method is novel in offering higher accuracy of measuring true CK-MB contents in human serum as compared to the conventional method. The possibility of accurately estimating CK-MB activity by our method which can inhibit MtCKs in healthy person and patient serum is likely to bring a break-through in clinical diagnostics.

Time course proteomic profile of rat acute myocardial infarction by SELDI-TOF MS analysis

Background Surface-enhanced laser desorption/ionization time of flight mass spectrometry (SELDI-TOF MS) is a powerful tool to detect biomarkers of many diseases. The purpose of this study is to evaluate SELDI-TOF MS as a potential tool for identifying serological biomarkers of acute myocardial infarction (AMI) at an early stage. Methods Serum samples were collected from rats after they had received left anterior descending coronary artery (LAD) ligation at 5, 15, 30, 60, 120, 240 and 360 min, respectively. These samples, along with serum samples from the sham-operated and uninjured control animals, were processed and analyzed with CM-10 ProteinChip and SELDI-TOF MS. Levels of myocardial creatine kinase isoenzyme MB (CKMB) activity and cardiac troponin I (cTnI) concentration were measured with respective commercial kits. Histological changes were examined after HE staining. Results Three peaks with m/ z 7586 Da, 7564 Da and 9583 Da, which were only found in the operated groups, were termed specific peaks. The peaks with m/ z 7586 and 7564 Da had the sensitivity of 97.0% and specificity of 97.0% in the ≥ 15 min operated groups. Four peaks with m/ z 4983, 5140, 8075, and 9423 Da were novel tissue unspecific injury related peaks in response to injury. Four peaks with m/ z 4400, 4542, 8400 and 7666 Da exhibited more than 2 fold peak height alterations. In contrast, the significant increase of CKMB activity and cTnI concentration in the serum could not be detected until 4 h after the ligation. Conclusions The specific peaks and unspecific injury related peaks detected by SELDI-TOF MS with CM-10 ProteinChip may be used as the biomarkers for early diagnosis of AMI.

Cardioprotective Effects of Bosentan, a Mixed Endothelin Type A and B Receptor Antagonist, during Myocardial Ischaemia and Reperfusion in Rats

The present study evaluated the cardioprotective potential of bosentan, a mixed endothelin type A and B receptor antagonist, in the myocardial ischaemia-reperfusion model of myocardial infarction. Adult male wistar rats (175-225 g) were divided into three groups: sham operated, non-myocardial ischaemia-reperfusion (SHAM); saline-treated myocardial ischaemia-reperfusion control (CON); bosentan-treated myocardial ischaemia-reperfusion (BOS). All animals were anaesthetized and subjected to 40 min. occlusion of left anterior descending coronary artery followed by 120 min. of reperfusion. Saline or drug was administered to the CON or BOS group, respectively, 20 min. after the left anterior descending coronary artery occlusion. Haemodynamic parameters viz. systolic arterial pressure, diastolic arterial pressure and heart rate were recorded throughout the experimental period. Hearts were subsequently excised and processed for histopathological and infarct size evaluation and for biochemical estimation of cardiac specific enzyme creatine kinase-MB (CK-MB) and myocardial malondialdehyde, a lipid peroxidation marker. Myocardial ischaemic reperfusion resulted in severe myocardial injury, depression of haemodynamic function, significant increase in malondialdehyde levels and decline in CK-MB isoenzyme activity in the heart tissue. Administration of bosentan (3 mg/kg, intravenously) slightly improved haemodynamic effects, decreased myocardial oxygen consumption, significantly (P<0.01) attenuated the rise in malondialdehyde levels and loss of myocardial CK-MB isoenzyme activity compared to the CON group, whereas bosentan administration significantly reduced the percentage area of fiber loss and infarct area. It is therefore concluded that endothelin-1 may mediate myocardial damage produced by ischaemia and reperfusion and that dual blockade of endothelinA and endothelinB receptors may have potential as a mode of therapy for myocardial infarction.

Ginsenosides compound (shen-fu) attenuates gastrointestinal injury and inhibits inflammatory response after cardiopulmonary bypass in patients with congenital heart disease

This study was undertaken to demonstrate that gastrointestinal mucosal injury occurs during cardiopulmonary bypass in children, increasing systemic inflammatory responses, and to determine whether shen-fu injection (the major components of which are ginsenosides compound, extract of Panax ginseng shown to have antioxidant properties) could attenuate gastrointestinal mucosal injury and subsequent inflammatory responses. Twenty-four children undergoing heart surgery for congenital heart defects were randomly assigned to groups C (placebo control, n = 12) and G (1.35 mg/kg ginsenosides compound intravenously before and throughout the course of cardiopulmonary bypass, n = 12). Central venous blood samples were taken before cardiopulmonary bypass and at 60 and 120 minutes after aortic declamping (reperfusion). Gastric intramucosal pH was measured by perioperative tonometry. Plasma lipid peroxidation product malondialdehyde, myocardium-specific creatine kinase isoenzyme MB activity, diamine oxidase, lipopolysaccharide, and interleukin 6 were all measured. Significant decrease in gastric intramucosal pH and increase in plasma diamine oxidase were seen during reperfusion in group C, accompanied by increases in plasma levels of malondialdehyde, lipopolysaccharide, interleukin 6, and creatine kinase isoenzyme MB (P < .01 vs before cardiopulmonary bypass). Shen-fu injection significantly attenuated these changes (P < .05). Consequently, fewer patients in group G (2/12) than in group C (7/12) needed postoperative inotropic support. Postoperative intensive care unit stay was shorter in group G than in group C. A tight positive correlation was seen between diamine oxidase and interleukin 6 at 60 minutes after aortic declamping and between diamine oxidase and lipopolysaccharide at 120 minutes after aortic declamping (r = 0.79, P < .0001). Ginsenosides compound may attenuate gastrointestinal injury and inhibit inflammatory response after cardiopulmonary bypass in patients with congenital heart disease.