scholarly journals PO-173 The Effects of Interval Exercise on oxidative stress and Smyd1-related myocardial hypertrophy in Rats with Myocardial Infarction

2018 ◽  
Vol 1 (4) ◽  
Author(s):  
Qiaoqin Liang ◽  
Mengxin Cai ◽  
Jiaqi Zhang ◽  
Zhenjun Tian
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Cardiac Function ◽  
Stress Level ◽  
Exercise Group ◽  
Control Group ◽  
Coronary Artery Ligation ◽  
Interval Exercise ◽  
Oxidative Stress Level ◽  
Sarcomere Assembly

Objective This study was carried out to investigate interval exercise on Smyd1 expression and F-actin sarcomere assembly in non-infarcted myocardium of normal and myocardial infarction(MI) rats and its possible mechanism. Methods Male SD rats were randomly divided into normal control group (C), normal interval exercise group (CE), sham-operated group (S), MI group (MI), MI with interval exercise group (ME) and MI with ROS Tempol group (MT), n=10. MI model was established by left anterior descending coronary artery ligation. Interval exercise was carried out on a small animal treadmill. MT group was given an oral solution of Tempol (2mmol/L). Hemodynamics was performed to evaluate cardiac function. HE and Masson staining were used to analyze the cross-sectional area (CSA) of cardiomyocytes and collagen volume fraction, respectively. T-SOD and MDA kits were used to detect oxidative stress. H9C2 cells were treated with H2O2. Immunofluorescence staining was used to determine Smyd1 expression and F-actin sarcomere assembly. RT-qPCR and Western blotting were used to detect the gene or protein expression of Smyd1, Trx1, Hsp90, MuRF1, cTnI, α-actinin and BNP. Results Smyd1, Trx1, Hsp90, MuRF1 and BNP expression in the peri-infarcted area were up-regulated, but cTnI and α-actinin expression and F-actin assembly were decreased. The cardiac function was reduced. Both interval exercise and Tempol intervention significantly increase the CSA and expression of Smyd1, Trx1, cTnI and α-actinin, improve the antioxidation capacity and F-actin sarcomere assembly and cardiac function, reduce the expression of Hsp90, MuRF1, BNP and ROS level, and inhibit the fibrosis of myocardium. The oxidative stress level was closely related to the Smyd1 expression. Improvement of cardiac function were correlated with Smyd1 expression. H2O2 can induce oxidative stress injuries of H9C2, and its closely related to cardiomyocytes oxidative stress level and Smyd1 expression. Conclusions Interval exercise could promote antioxidant capability and physiological cardiomyocyte hypertrophy, regulate the expression of Smyd1, Hsp90 and MuRF1 in infarcted heart; so as to improve the cardiac function. Smyd1 may participate in pathologic hypertrophy of cardiomyocytes caused by oxidative stress.

Abstract 2879: Targeted and Tailored: A New Approach to Regeneration after a Myocardial Infarction

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Hiroko Fujii ◽  
Shu-Hong Li ◽  
Yasuo Miyagi ◽  
Shafie Fazel ◽  
Terrence M Yau ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Perfusion ◽  
Cardiac Function ◽  
Border Zone ◽  
Control Group ◽  
Vascular Density ◽  
Coronary Artery Ligation ◽  
New Approach ◽  
Cell Counts ◽  
Targeted Ultrasound

Rationale: Targeted: Ultrasound targeted microbubble destruction (UTMD) delivers genes directly to the injured myocardium. Tailored: UTMD could permit recurrent treatment until recovery is complete. Hypothesis: Repeated UTMD is a novel strategy to induce tissue regeneration and improve ventricular function after a myocardial infarction. Methods: Microbubbles were mixed with plasmids containing stem cell factor (SCF) and stromal cell-derived factor (SDF)-1α genes. Seven days after coronary artery ligation, adult rats underwent UTMD either 1, 3 or 6 times at 2-day intervals in 4 randomly assigned groups: Control group: 6 UTMD treatments with empty plasmid (n=4); Repeat 1 (n=6), Repeat 3 (n=7), Repeat 6 (n=6) groups: 1, 3 or 6 treatments, respectively, of UTMD with SCF and SDF-1α plasmid DNA. Cardiac function (echocardiography) and myocardial perfusion (myocardial contrast echocardiography) were assessed on days 0, 10 and 24 after the first treatment. Biochemical assessments were performed on day 24. Results: Cardiac function was highest in the Repeat 6 group (p<0.05 vs. Repeat 1). Myocardial SCF levels were higher after multiple rather than single UTMD treatments (p<0.05 for Repeat 3 and Repeat 6 vs. Repeat 1), with the highest levels in the Repeat 6 group (p<0.05 vs. Repeat 3). Myocardial SDF-1α levels and c-kit-positive cell counts also increased with the maximum number of treatments (p<0.05 for Repeat 6 vs. Repeat 1). Myocardial CXCR4-positive cells were more numerous in the remote regions of both multiple UTMD groups (p<0.05 for Repeat 3 and Repeat 6 vs. Repeat 1). Both myocardial perfusion in the infarct region and vascular density (Factor VIII or alpha-smooth muscle actin staining) in the border zone increased with repeated treatments (p<0.05 for Repeat 3 and Repeat 6 vs. Repeat 1), with an additional increase in the Repeat 6 group (p<0.01 vs. Repeat 3). Conclusions: Targeted ultrasound delivery of SCF and SDF-1α genes to the myocardium induced angiogenesis, recruited progenitor cells and improved cardiac function. Multiple UTMD treatments further enhanced regeneration. Tailoring the treatment by providing the number of interventions required to restore function provides a new approach to cardiac regeneration following a myocardial infarction.

scholarly journals Scavenging superoxide selectively in mouse forebrain is associated with improved cardiac function and survival following myocardial infarction

2009 ◽  
Vol 296 (1) ◽  
pp. R1-R8 ◽  
Author(s):  
Timothy E. Lindley ◽  
David W. Infanger ◽  
Mark Rishniw ◽  
Yi Zhou ◽  
Marc F. Doobay ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Central Nervous System ◽  
Nervous System ◽  
Gene Transfer ◽  
Cardiac Function ◽  
Myocardial Function ◽  
Critical Role ◽  
Coronary Artery Ligation ◽  
Control Vector

Dysregulation in central nervous system (CNS) signaling that results in chronic sympathetic hyperactivity is now recognized to play a critical role in the pathogenesis of heart failure (HF) following myocardial infarction (MI). We recently demonstrated that adenovirus-mediated gene transfer of cytoplasmic superoxide dismutase (Ad-Cu/ZnSOD) to forebrain circumventricular organs, unique sensory structures that lack a blood-brain barrier and link peripheral blood-borne signals to central nervous system cardiovascular circuits, inhibits both the MI-induced activation of these central signaling pathways and the accompanying sympathoexcitation. Here, we tested the hypothesis that this forebrain-targeted reduction in oxidative stress translates into amelioration of the post-MI decline in myocardial function and increase in mortality. Adult C57BL/6 mice underwent left coronary artery ligation or sham surgery along with forebrain-targeted gene transfer of Ad-Cu/ZnSOD or a control vector. The results demonstrate marked MI-induced increases in superoxide radical formation in one of these forebrain regions, the subfornical organ (SFO). Ad-Cu/ZnSOD targeted to this region abolished the increased superoxide levels and led to significantly improved myocardial function compared with control vector-treated mice. This was accompanied by diminished levels of cardiomyocyte apoptosis in the Ad-Cu/ZnSOD but not the control vector-treated group. These effects of superoxide scavenging with Ad-Cu/ZnSOD in the forebrain paralleled increased post-MI survival rates compared with controls. This suggests that oxidative stress in the SFO plays a critical role in the deterioration of cardiac function following MI and underscores the promise of CNS-targeted antioxidant therapy for the treatment of MI-induced HF.

Abstract 250: Pericardial Grafting Of Cardiac Progenitor Cells In The Three-dimensional Thick Scaffold Improves Cardiac Function After Myocardial Infarction In Mice.

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Naomichi Kondo ◽  
Toshio Nagai ◽  
Mei-Lan Liu ◽  
Toshinao Takahashi ◽  
Masato Kanda ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Treatment Group ◽  
Cardiac Function ◽  
Three Dimensional ◽  
Control Group ◽  
Coronary Artery Ligation ◽  
Fish Analysis ◽  
Artery Ligation ◽  
Self Assembling ◽  
Graft Area

Cardiac progenitor cell (CPC) therapy for heart disease has been examined enthusiastically. However, optimal scaffolds which maintain the transplanted cells are still elusive. We used clonally expanded stem cell antigen 1-positive CPCs from adult mice and produced a three-dimensional thick scaffold (CPC-scaffold), in which CPCs were cultivated up to 2 month with self-assembling peptide RADA16-I. Addition of designer self-assembling peptide containing the active motifs of 2-unit RGD binding sequence and IGF-1 promoted three-dimensional spreading and viability of CPCs. After making myocardial infarction (MI) with left coronary artery ligation in mice, we transplanted CPC-scaffold on the surface of infarction area and confined it inside of the pericardial space by closing parietal pericardium. Four weeks after transplantation, echocardiography showed that FS of treatment group (16±10%, n=17) was higher than that of control (MI only) group (10±6.8%, n=19) (P<0.05) and that LVDd of treatment group (5.4±1.0mm, n=17) was smaller than that of control group (6.2±1.1mm, n=19) (P<0.05). Infarction area was significantly decreased in treatment group (46±21%, n=17), compared to control group (59±19%, n=18) (P<0.05). Immunohistochemical staining for von-Willebrand factor (vWF) showed that the number of vWF-positive capillaries per mm2 in treatment group (16.8±3.2, n=5) was higher than that of control group(8.9±3.4, n=5) (P<0.05). There were many of CD31-positive capillaries with or without α-smooth muscle cell actin-expressing perivascular cells in the graft area. By using fluorescent-conjugated avidin, biotin-labeled scaffold was globally detected in the graft area 1 week after transplantation, but sparsely 4weeks after, suggesting that the transplanted scaffold was biodegradable. To examine whether transplanted CPCs remain in the scaffold, we labeled CPCs with red fluorescence protein (RFP). RFP+CPCs were observed in the graft area 4 weeks after transplantation of RFP+CPC-scaffold. FISH analysis showed that sex-mismatched CPCs were globally detected in the graft area on the surface of the heart. Therefore pericardial grafting of well-vascularized and cellularized CPC-scaffold was a useful method to improve cardiac function after MI.

scholarly journals Exercise Capacity is Improved by Levosimendan in Heart Failure and Sarcopenia Mice via the Alleviation of Atrophy and Apoptosis of Skeletal Muscle

2021 ◽  
Author(s):  
Di Wang ◽  
Ming Song ◽  
Long-fei Shen ◽  
Lu Han ◽  
Ping Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Membrane Potential ◽  
Cardiac Function ◽  
Mitochondrial Membrane Potential ◽  
Exercise Capacity ◽  
Stress Level ◽  
Mitochondrial Membrane ◽  
Oxidative Stress Level

Abstract Background Sarcopenia, a common complication of heart failure (HF), dramatically reduces the benefits of exercise training. Levosimendan is an effective drug for the treatment of heart failure, but its relationship with sarcopenia is still unclear. We aimed to investigate the effect of levosimendan on heart failure with sarcopenia and to explore whether levosimendan can enhance skeletal muscle contractibility, improve skeletal muscle atrophy, and thus improve exercise tolerance of individuals with heart failure.Methods C57BL6/J mice were used to establish the heart failure with sarcopenia model by ligating of the left anterior descending branch combined with hindlimb unloading and were injected of levosimendan (3mg/Kg, once a week, four times in total). Mice (n=40) were divided into control group, sham operation group, HF group, HF + solvent group, HF + levosimendan group, HF + sarcopenia group, HF + sarcopenia + solvent group, HF+ sarcopenia + levosimendan group. After the treatment, exercise capacity and cardiac function were evaluated. Serum BNP, LDH, and CK content were measured. Muscle morphology, fiber type, inflammation level, and apoptosis levels were detected by histopathological and molecular biological methods. Mitochondrial function and oxidative stress level were assessed by mitochondrial membrane potential and SOD activity.Result Levosimendan could improve EF and FS in mice with HF and sarcopenia (P<0.001) and increase their forelimb grip strength, hanging impulse, maximum running distance and time (P<0.05). After correcting for EF, the improvement of exercise capacity by levosimendan remained (P<0.05). HE staining showed that levosimendan directly increased the CSA of gastrocnemius in mice with HF and sarcopenia (P<0.001). After levosimendan injection, the proportion of slow muscle fibers increased, but this improvement of muscle fiber typing might be attributed to improved cardiac function (P>0.05). Levosimendan also maintained mitochondrial membrane potential, decreased cleaved caspase-3, cleaved caspase-9, Bax expression, and increased Bcl2 expression (P<0.05). This effect is independent of improved cardiac function. IL-6, TNF-α expression decreased and SOD activity, GSH/GSSG ratio significantly increased (P<0.05) in skeletal muscle after injection of levosimendan, improved oxidative stress level. The improvement in oxidative stress level was attributed to improved cardiac function (P>0.05).Conclusion Levosimendan reduce the loss of skeletal muscle mitochondrial membrane potential, decrease the apoptosis, alleviate the inflammation and oxidative stress, and ultimately improve the exercise capacity of mice with heart failure and sarcopenia. Therefore, levosimendan may be a potential drug for the treatment of heart failure with sarcopenia.

Development of the Express Method for Determining the Oxidative Stress Level of the Population

Food Industry ◽  
2018 ◽  
Vol 3 (4) ◽  
Author(s):  
Ekaterina V. Pastushkova ◽  
Olga V. Chugunova ◽  
Leonid S. Volkanin
Keyword(s):  
Oxidative Stress ◽  
Stress Level ◽  
Express Method ◽  
Oxidative Stress Level

Abstract 17166: Myeloid-specific Deletion of the Glucocorticoid Receptor Increases Mitochondrial Oxidative Stress and Impairs Wound Healing After Myocardial Infarction

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Jonas Neuser ◽  
Daniela Fraccarollo ◽  
Jan P Tuckermann ◽  
Paolo Galuppo ◽  
Johann Bauersachs
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Wound Healing ◽  
Glucocorticoid Receptor ◽  
Mononuclear Cells ◽  
Flow Cytometric Analysis ◽  
Myeloid Cells ◽  
Coronary Artery Ligation ◽  
Mitochondrial Oxidative Stress ◽  
Specific Deletion

Background: Glucocorticoid administration impairs ischemic wound healing by inhibiting inflammation and angiogenesis via a glucocorticoid receptor (GR)-mediated transcriptional response. However, there are also apparently contradictory reports claiming protective effects of glucorticoid administration after myocardial infarction (MI). We investigated the role of the GR in myeloid cells for infarct wound healing, using GR deficient mice (GRLysMCre). Methods and Results: MI was induced by permanent left coronary artery ligation in GRflox (wild-type [WT] controls) and GRLysMCre mice. The 7-day mortality was significantly lower in WT compared with GRLysMCre mice. At 7 days post MI, GRLysMCre mice exhibited significantly enhanced thinning and dilatation of the infarcted wall, LV chamber enlargement and functional deterioration. This was associated with altered granulation tissue formation and impaired neoangiogenesis at the site of ischemic injury. Multicolor flow cytometric analysis and immunohistochemical studies revealed at the 2nd day post infarction less infiltrating mononuclear cells [CD11bhigh and (CD49b, NK1.1, B220, CD90, Ly6G)low] in the healing myocardium of GRLysMCre mice. Mononuclear cells were identified as monocytes (F4/80, I-Ab, CD11c)low and as macrophages/dendritic cells (F4/80, I-Ab, CD11c)high. Monocytes lacking GR, isolated from peripheral blood and spleen by magnetic-activated cell sorting 1 day after MI, displayed reduced migration capacity and increased superoxide anion production in mitochondria, which was detected by HPLC-electrochemical analysis of Mito-2-hydroxy-E+. Moreover, at day 2 and 3 we found enhanced cellular and mitochondrial oxidative stress in the healing myocardium of GRLysMCre mice. Conclusions: Myeloid-specific deletion of the GR increasing mitochondrial oxidative stress alters wound healing and promotes infarct expansion. Our results suggest that the GR in myeloid cells play a crucial role during cardiac repair after myocardial infarction.

Abstract 177: Ticagrelor, but not Clopidogrel, Protects the Heart Against Reperfusion Injury and Improves Remodeling After Myocardial Infarction

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Yumei Ye ◽  
Jose R Perez-Polo ◽  
Manjyot K Nanhwan ◽  
Sven Nylander ◽  
Yochai Birnbaum
Keyword(s):  
Myocardial Infarction ◽  
Platelet Aggregation ◽  
Reperfusion Injury ◽  
Heart Function ◽  
Oral Treatment ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Coronary Artery Ligation ◽  
Ventricular Ejection Fraction

Background: Clopidogrel (C) and Ticagrelor (T) are P2Y12 ADP receptor antagonists. In addition, ticagrelor inhibits adenosine cell uptake. In PLATO trial T reduced the incidence of the primary composite endpoint myocardial infarction, stroke or cardiovascular death over C in patients with acute coronary syndromes. Previous data show that 7d pretreatment with T limits infarct size (IS) in rats. We compared the effects of C and T, administered just before reperfusion on IS. We also assessed the effect of T and C, administered just before reperfusion and/or 6w oral treatment on cardiac remodeling. Methods: Rats underwent 30min coronary artery ligation. 1) At 25min of ischemia rats received intraperitoneal (IP) vehicle, T (10 or 30mg/kg), or C (12.5mg/kg). Area at risk (AR) was assessed by blue dye and IS by TTC staining 24h after reperfusion. 2) Rats received vehicle without (sham) or with (control) coronary ischemia, T (30mg/kg) IP (TIP), T (300mg/kg/d) oral for 6w, started a day after reperfusion (TPO), TIP+PO (TIPPO), or C (12.5mg/kg IP +62.5mg/kg/d PO for 6w). LV dimensions and function was assessed by echo at 6w. Results: 1) AR was comparable among groups. IS was 45.3±1.7% of the AR in the control group. T10 (31.5±1.8%; p=0.001) and T30 (21.4±2.6% p<0.001) significantly reduced IS, whereas C (42.4±2.6%) had no effect. Platelet aggregation in the controls was 64.7±1.3% and was comparable in T30 (24.9±1.8%) and C (23.2±1.8%) at 2h post reperfusion. T30 increased Akt, eNOS and ER1/2 phosphorylation 4h after reperfusion, whereas C had no effect. 2) Platelet aggregation at 1w oral treatment was 59.7±3.2% in the control group and was comparable in TIPPO (18.1±1.3%) and C (17.4±0.7%). Left ventricular ejection fraction was 77.6±0.9%*, 44.8±3.5%, 69.5±1.6%*, 69.2±1.0%*, 76.3±1.2%*, and 37.4±3.7% in the sham, vehicle, TIP, TPO, TIPPO and C treated group, respectively (*p<0.001 vs. vehicle). Left ventricular diameters at diastole and systole showed the same pattern. Conclusions: T, but not C, administered just before reperfusion protects against reperfusion injury. Oral T (in combination or not with acute treatment just before reperfusion) treatment for 6w improves heart function. C, despite achieving similar degree of platelet inhibition had no effect on remodeling.

scholarly journals PHYSICAL EXERCISE ON THE RECOVERY OF OBESITY MYOCARDIAL INFARCTION

2021 ◽  
Vol 27 (8) ◽  
pp. 783-785
Author(s):  
Mian Wang ◽  
Fan Wu
Keyword(s):  
Quality Of Life ◽  
Myocardial Infarction ◽  
Physical Exercise ◽  
Nursing Intervention ◽  
Exercise Group ◽  
Control Group ◽  
Level Of Evidence ◽  
Early Exercise ◽  
Physical Functions

ABSTRACT Introduction: Myocardial infarction caused by human obesity can cause a decline in mobility and a decline in the quality of a healthy life. Sports training is beneficial to maintain early physical functions after myocardial infarction. Objective: This article deals with the effect of applying walking aerobic exercise in the rehabilitation treatment of patients with myocardial infarction. Methods: We enrolled 91 patients with myocardial infarction in the early exercise group and 90 patients in the control group. The control group received the routine nursing intervention, and the early exercise group received early physical exercise rehabilitation therapy. Results: The actual quality of life of the early exercise group was higher than that of the control group. The incidence of cardiovascular adverse events was lower than that of the control group. Conclusion: Physical exercise therapy used in acute myocardial infarction can reduce adverse cardiovascular events and improve the quality of life of patients. Level of evidence II; Therapeutic studies - investigation of treatment results.

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