Dapagliflozin Improves Cardiac Function, Remodeling, Myocardial Apoptosis, and Inflammatory Cytokines in Mice with Myocardial Infarction

2021 ◽  
Author(s):  
Kai Wang ◽  
Zhongming Li ◽  
Yan Sun ◽  
Xianling Liu ◽  
Wenjie Ma ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Inflammatory Cytokines ◽  
Myocardial Apoptosis

Effects of Blood Purification on Serum Levels of Inflammatory Cytokines and Cardiac Function in a Rat Model of Sepsis

2017 ◽  
Vol 44 (1) ◽  
pp. 40-50
Author(s):  
Cong-Meng Lin ◽  
Cun-Rong Chen ◽  
Xue-Qiong Wu ◽  
Jin-Hua Ren ◽  
Shao-Zhen Chen ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Inflammatory Cytokines ◽  
Rat Model ◽  
Serum Levels ◽  
Blood Purification ◽  
Sham Operation ◽  
Sham Treatment ◽  
Treatment Groups ◽  
Myocardial Apoptosis ◽  
Cardiac Functions

Objective: The study aimed to explore the effects of blood purification (BP) on serum levels of inflammatory cytokines and cardiac function in a rat model of sepsis. Methods: A rat model of sepsis was established by cecal ligation and puncture. All rats were divided into the normal control, sham operation, model, sham treatment, and BP treatment groups. Cardiac functions, inflammatory cytokines, myocardial enzymes, pathological score of cardiac muscle tissue, and myocardial apoptosis of rats in each group were compared. Results: Sepsis rats had higher serum levels of inflammatory cytokines and lower cardiac function than those in the normal control and sham operation groups. Compared with the model and sham treatment groups, improved cardiac functions, decreased inflammatory cytokines, myocardial enzymes, pathological score, and myocardial apoptosis and mortality were observed in the BP treatment group. Conclusion: BP may reduce serum levels of inflammatory cytokines and improve cardiac function of sepsis rats.

Abstract 162: c-fos Protects the Myocardium from Ischemic Injury and Improves Cardiac Function

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Xiangru Lu ◽  
Ming Lei ◽  
Fuli Xiang ◽  
Qingping Feng
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Infarct Size ◽  
Ischemic Injury ◽  
Coronary Artery Ligation ◽  
Area At Risk ◽  
Artery Ligation ◽  
Protein Ratio ◽  
Myocardial Apoptosis ◽  
Bax Protein

Background: c-fos is an immediate early response gene. c-Fos proteins form heterodimers with Jun family proteins, and the resulting AP-1 complexes regulate transcription by binding to the AP-1 sequence found in many cellular genes. c-fos is activated in cardiomyocytes following myocardial infarction. However, the role of c-fos in regulating cardiomyocyte survival and cardiac function post myocardial infarction (MI) is not known. In the present study, we hypothesized that c-fos protects the myocardium from ischemic injury and improves cardiac function. Methods and Results: The generation of mice with cardiomyocyte specific c-fos −/ − was achieved by crossing the floxed c-fos mice with mice over-expressing Cre recombinase under the control of α-myosin heavy chain. Wild-type (WT) littermates were used as controls. MI was induced by coronary artery ligation. Infarct size, myocardial apoptosis and cardiac function were determined at 2 days post-MI. While area at risk was similar between the 2 groups, infarct size was significantly increased in c-fos −/ − compared to WT mice (58 ± 4% vs. 44 ± 3%, P< 0.05). Myocardial caspase-3 activity and cytosolic DNA fragments in the peri-infarct region were significantly increased while Bcl-2/Bax protein ratio was significantly decreased in c-fos −/− mice ( P< 0.05). LV pressure volume relationship was assessed in vivo using a Millar pressure conductance catheter. LV end-systolic elastance ( E es ) and +d P /dt max were significantly decreased in c-fos −/− compared to WT mice (1.7 ± 0.4 vs. 5.1 ± 1.0 mmHg/μL; 4776 ± 567 vs. 7006 ± 319 mmHg/s, P< 0.01). Conclusions: Deficiency in c-fos increases infarct size and myocardial apoptosis leading to impaired cardiac function post-MI. Our results suggest that c-fos protects the myocardium from ischemic injury and improves cardiac function.

Cortistatin Improves Cardiac Function After Acute Myocardial Infarction in Rats by Suppressing Myocardial Apoptosis and Endoplasmic Reticulum Stress

2016 ◽  
Vol 22 (1) ◽  
pp. 83-93 ◽  
Author(s):  
Zhi-Yu Shi ◽  
Yue Liu ◽  
Li Dong ◽  
Bo Zhang ◽  
Meng Zhao ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Endoplasmic Reticulum ◽  
Cardiac Function ◽  
Er Stress ◽  
Rat Model ◽  
Caspase 3 ◽  
Apoptotic Pathway ◽  
Myocardial Apoptosis ◽  
Glucose Regulated Protein

Objectives: The endoplasmic reticulum (ER) stress-induced apoptotic pathway is associated with the development of acute myocardial infarction (AMI). Cortistatin (CST) is a novel bioactive peptide that inhibits apoptosis-related injury. Therefore, we investigated the cardioprotective effects and potential mechanisms of CST in a rat model of AMI. Methods: Male Wistar rats were randomly divided into sham, AMI, and AMI + CST groups. Cardiac function and the degree of infarction were evaluated by echocardiography, cardiac troponin I activity, and 2,3,5-triphenyl-2H-tetrazolium chloride staining after 7 days. The expression of CST, ER stress markers, and apoptotic markers was examined using immunohistochemistry and Western blotting. Results: Compared to the AMI group, the AMI + CST group exhibited markedly better cardiac function and a lower degree of infarction. Electron microscopy and terminal deoxynucleotidyl transferase dUTP nick end labeling confirmed that myocardial apoptosis occurred after AMI. Cortistatin treatment reduced the expression of caspase 3, cleaved caspase 3, and Bax (proapoptotic proteins) and promoted the expression of Bcl-2 (antiapoptotic protein). In addition, the reduced expression of glucose-regulated protein 94 (GRP94), glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding proteins homologous protein, and caspase 12 indicated that ER stress and the apoptotic pathway associated with ER stress were suppressed. Conclusions: Exogenous CST has a notable cardioprotective effect after AMI in a rat model in that it improves cardiac function by suppressing ER stress and myocardial apoptosis.

scholarly journals Effect of Tirofiban Injection on vascular endothelial function, cardiac function and inflammatory cytokines in patients with acute myocardial infarction after emergency Percutaneous Coronary Intervention

2021 ◽  
Vol 38 (1) ◽  
Author(s):  
Shi-xin Kang ◽  
Xiao-min Meng ◽  
Jing Li
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Endothelial Function ◽  
Cardiac Function ◽  
Inflammatory Cytokines ◽  
Control Group ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Significant Difference ◽  
Experimental Group

Objectives: To evaluate the effect of tirofiban injection on vascular endothelial function, cardiac function, inflammatory cytokines and other indicators in patients with acute myocardial infarction after emergency PCI and its clinical significance. Methods: Eighty patients with acute myocardial infarction admitted to Affiliated Hospital of Hebei University from March 18, 2020 to October 18, 2020 were enrolled and randomly divided into two groups: the experimental group and the control group, with 40 cases in each group. Patients in both groups underwent PCI. Patients in the control group were given oxygen inhalation, monitoring, and basic medications for myocardial infarction, such as nutritional myocardial drugs, statins, aspirin, nitrates, clopidogrel, and β-blockers. In contrast, patients in the experimental group received tirofiban 10 ug/kg intravenously over 5min immediately before PCI in addition to basic treatment, and then tirofiban 0.1 ug/(kg/min) was pumped via intravenous pump postoperatively for 48 hour. The changes of vascular endothelial function, cardiac function and adverse drug reactions (ADRs) in the two groups before treatment, one week and one month after treatment, as well as changes of inflammatory cytokines such as CRP and IL-6 in the two groups before and after treatment were compared and analyzed. Results: Compared with the control group, FMD, NO, ET-1 and other indexes in the experimental group were significantly improved one week and one month after treatment, with statistically significant differences (p<0.05). BNP, LVEDD, LVEF and additional indexes in the experimental group were significantly lower than those in the control group at one week and one month after treatment, with statistically significant differences (p=0.00). Moreover, the incidence of ST-segment fallback > 70% in the experimental group was 72.5% after treatment, which was significantly better than that of 47.5% in the control group, with a statistically significant difference (p=0.03). CRP and IL-6 in the experimental group were significantly lower than those in the control group after treatment, with a statistically significant difference (p=0.00). There was no statistical significance in the incidence of ADRs between the two groups after treatment (p=0.42). Conclusion: Tirofiban injection after emergency PCI is a beneficial treatment regime for patients with STEMI. With such a treatment regime, cardiac function and vascular endothelial function of patients can be dramatically improved, coronary blood supply will be ameliorated, inflammatory cytokines can be reduced, and no significant increase can be seen in the incidence of adverse reactions. doi: https://doi.org/10.12669/pjms.38.1.4413 How to cite this:Kang S, Meng X, Li J. Effect of Tirofiban Injection on vascular endothelial function, cardiac function and inflammatory cytokines in patients with acute myocardial infarction after emergency Percutaneous Coronary Intervention. Pak J Med Sci. 2022;38(1):---------. doi: https://doi.org/10.12669/pjms.38.1.4413 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

scholarly journals PO-190 Exercise Training Protects Against Cardiac Pathological Remodeling in Myocardial Infarction rats via Improving Mitochondrial Biogenesis

2018 ◽  
Vol 1 (4) ◽  
Author(s):  
Dandan Jia ◽  
Zhenjun Tian
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Exercise Training ◽  
Cardiac Function ◽  
Myocardial Fibrosis ◽  
Mitochondrial Biogenesis ◽  
Cardiac Dysfunction ◽  
Myocardial Apoptosis ◽  
The Impact ◽  
Pathological Remodeling

Objective  Growing evidence suggests that exercise training reverses cardiac pathological remodeling and cardiac dysfunction during myocardial infarction (MI), but the underlying mechanisms have not been fully understood. In this study, we investigated the impact of exercise training on cardiac function, myocardial fibrosis, apoptosis, oxidative stress and mitochondrial biogenesis. Methods Sprague Dawley rats were subjected to MI by permanent ligation of the left anterior descending (LAD) coronary artery or Sham operation. Rats with MI were randomly assigned to sedentary MI group (MI) and MI with exercise training group (MI+EX), and compared to sham-operated group (Sham). Haemodynamics and Masson staining were conducted to evaluate the effect of exercise training on cardiac function and myocardial fibrosis. Myocardial apoptosis, oxidative stress, mitochondrial biogenesis and molecular signaling mechanism were analyzed. Results  Exercise training significantly improves cardiac function and mitigates the MI-induced cardiac pathological remodeling. Meanwhile, Exercise training significantly attenuates MI-induced apoptosis, oxidative stress and mitochondrial biogenesis. In addition, activation of PI3K pathway following MI is further induced by exercise training. Conclusions  Exercise training protects against MI-induced cardiac dysfunction and pathological remodeling through preventing myocardial apoptosis and oxidative stress, and enhancing mitochondrial biogenesis.

scholarly journals Silencing CircHIPK3 Sponges miR-93-5p to Inhibit the Activation of Rac1/PI3K/AKT Pathway and Improves Myocardial Infarction-Induced Cardiac Dysfunction

2021 ◽  
Vol 8 ◽  
Author(s):  
Yijin Wu ◽  
Min Wu ◽  
Jue Yang ◽  
Ying Li ◽  
Wenying Peng ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Infarct Size ◽  
Cardiac Dysfunction ◽  
Harmful Effect ◽  
Akt Pathway ◽  
Circular Rnas ◽  
Cerna Network ◽  
Myocardial Apoptosis

The ceRNA network involving circular RNAs (circRNAs) is essential in the cardiovascular system. We investigated the underlying ceRNA network involving circHIPK3 in myocardial infarction (MI). After an MI model was established, cardiac function was verified, and myocardial tissue damage in mice with MI was evaluated. A hypoxia model of cardiomyocytes was used to simulate MI in vivo, and the expression of and targeting relationships among circHIPK3, miR-93-5p, and Rac1 were verified. The apoptosis of cardiomyocyte was identified. Gain- and loss-of-functions were performed to verify the ceRNA mechanism. The MI-modeled mice showed cardiac dysfunction and enlarged infarct size. CircHIPK3 was highly expressed in mouse and cell models of MI. Silencing circHIPK3 reduced infarct size, myocardial collagen deposition, and myocardial apoptosis rate and improved cardiac function. CircHIPK3 sponged miR-93-5p, and miR-93-5p targeted Rac1. Overexpression of miR-93-5p inhibited MI-induced cardiomyocyte injury and eliminated the harmful effect of circHIPK3. CircHIPK3 acted as ceRNA to absorb miR-93-5p, thus promoting the activation of the Rac1/PI3K/AKT pathway. We highlighted that silencing circHIPK3 can upregulate miR-93-5p and then inhibit the activation of Rac1/PI3K/Akt pathway, which can improve MI-induced cardiac dysfunction.

scholarly journals PO-163 Aerobic exercise activates myocardial FGF21/FGFR1/PI3K-AKT signaling pathway and inhibits cardiomyocyte apoptosis in post-myocardial infarction rats

2018 ◽  
Vol 1 (4) ◽  
Author(s):  
Mingxiao Li ◽  
Zhenjun Tian
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Aerobic Exercise ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Collagen Fibers ◽  
Cardiomyocyte Apoptosis ◽  
Akt Pathway ◽  
Akt Signaling Pathway ◽  
Myocardial Apoptosis

Objective To investigate the effect of aerobic exercise on the expression of fibroblast growth factor 21 (FGF21) and cardiomyocyte apoptosis in Myocardial Infarction (MI) rats. Methods male SD rats were randomly divided into three groups：the sham operation (S), sedentary MI group (MI) and MI with aerobic exercise group (ME). The MI model was established by ligation of the left anterior descending branch of the left coronary artery. ME group were trained four weeks after the operation. LVSP, LVEDP and ±dp/dtmax were used to evaluate cardiac function. H9C2 cardiomyocytes were stimulated by 400 μmol/L H2O2 for 4h to simulate myocardial apoptosis mode. AMPK agonist AICAR and FGF21 receptor inhibitor PD166866 were used to interfere with H9C2. Myocardial collagen volume fraction was calculated by Masson staining and myocardium FGF21, FGFR1, Bax, Bcl-2 and PI3K-AKT pathway by western blotting or RT-Qpcr. Cardiomyocytes apoptosis was evaluated by TUNEL. Results Compared with S, the expression of FGF21, FGFR1, Bax, Bcl-2 and PI3K, AKT increased significantly in MI group, the apoptotic cardiomyocytes and collagen fibers increased significantly, but the cardiac function decreased. Compared to MI, myocardium FGF21, FGFR1 and PI3K, AKT were further increased in ME group, the Bax/Bcl-2 and the apoptotic cardiomyocytes decreased significantly. The percentage of collagen fibers decreased and the cardiac function was improved. Myocardium FGF21 was positively correlated with the inhibition of cardiomyocyte apoptosis and the improvement of cardiac function. Furthermore, the expression of Bax/Bcl-2, TNF-α/IL-10 and the apoptotic cardiomyocytes was significantly increased by PD166866, but PI3K-AKT pathway decreased significantly by PD166866. However, AICAR single intervention or PD166866 simultaneous intervention also can reverse this adverse effects. Conclusions Exercise can increase myocardial FGF21/FGFR1 with MI. The one of the mechanisms is to activate PI3K-AKT pathway to inhibit cardiaomyocyte apoptosis and inflammatory. It indicates that FGF21/FGFR1/PI3K-AKT signaling pathway plays an important role in inhibiting myocardial apoptosis and improving cardiac function.

scholarly journals Hepatocyte growth factor intervention to reduce myocardial injury and improve cardiac function on diabetic myocardial infarction rats

2020 ◽  
Vol 64 (s2) ◽  
Author(s):  
Zaiyong Zhang ◽  
Cheng Long ◽  
Yufeng Guan ◽  
Mingcai Song
Keyword(s):  
Myocardial Infarction ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cardiac Function ◽  
Ventricular Remodeling ◽  
Myocardial Cell ◽  
Diabetic Rats ◽  
Control Group ◽  
Myocardial Apoptosis ◽  
Hepatocyte Growth

Acute myocardial infarction (AMI) is recognized to be a severe threat to people’s health conditions and life quality. The accumulation of hepatocyte growth factor (HGF) in ischemic myocardium has been observed in both processes of experimental ischemia and reperfusion (I/R) and permanent coronary artery occlusion. The aim of the study was to investigate the effect of HGF on myocardial cell apoptosis, ventricular remodeling and cardiac function after myocardial infarction (MI) in diabetic rats, and to explore whether the effect is mediated by HGF/c-Met signaling pathway. MI significantly increases LVWI and RVWI and myocardial apoptotic index, and up-regulates the expression of HGF and c-Met at mRNA and protein levels in MI control group. The LVWI and RVWI, and myocardial apoptosis were reduced by treatment with HGF, which also increased the myocardial cell viability and the expression of HGF and c-Met. In summary, HGF significantly attenuates myocardial apoptosis and improves cardiac function after AMI in diabetic rats by further enhancing the activation of HGF/c-Met pathway.

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