ribonucleic acid/infarzierung

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Expression and modulation of steroidogenic acute regulatory protein messenger ribonucleic acid in rat cardiocytes and after myocardial infarction.

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We examined whether the mRNA for steroidogenic acute regulatory (StAR) protein, a crucial factor in the rate-limiting step of aldosterone biosynthesis, is expressed and regulated in rat heart. We performed quantitative RT-PCR for StAR mRNA in an in vitro and an in vivo model: purified rat neonatal

3-N-butylphthalide inhibits neuronal apoptosis in rats with cerebral infarction via targeting P38/MAPK.

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To study the effect of 3-n-butylphthalide (NBP) on neuronal apoptosis in rats with cerebral infarction (CI) through the p38/mitogen-activated protein kinase (MAPK) pathway.A total of 30 rats were divided into control group (healthy rats, n=10), model group

Relationship between NogoA/NgR1/RhoA signaling pathway and the apoptosis of cerebral neurons after cerebral infarction in rats.

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The aim of this study was to investigate the effect and the mechanism of the NogoA/NgR1/RhoA signaling pathway on the apoptosis of neurons in cerebral infarction (CI) rats. Our findings might provide references for clinical prevention and treatment of CI.A

Effect of acupuncture on neurovascular units after cerebral infarction in rats through PI3K/AKT signaling pathway.

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To study the effect of acupuncture on neurovascular units after cerebral infarction (CI) in rats through the phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/AKT) signaling pathway.A total of 36 Sprague-Dawley rats were randomly divided into

MiR-29 inhibits neuronal apoptosis in rats with cerebral infarction through regulating Akt signaling pathway.

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The aim of this study was to explore the influence of micro ribonucleic acid (miR)-29 on neuronal apoptosis in rats with cerebral infarction by regulating the protein kinase B (Akt) signaling pathway.A total of 36 Sprague-Dawley rats were randomly divided

Comparison of cardioprotective effects of salvianolic acid B and benazepril on large myocardial infarction in rats.

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In the present study, we compared cardioprotective effects of salvianolic acid B (Sal B) and the angiotension-converting enzyme inhibitor, benazepril, in rats with large myocardial infarction (MI). The large MI was produced by coronary artery ligation for 4 weeks in rats. The rats were divided into

Role and mechanism of microRNA-548c-3p/c-Myb in myocardial infarction fibrosis in rats.

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To investigate the role of micro ribonucleic acid (miR)-548c-3p in myocardial fibrosis after myocardial infarction (MI), and to explore the possible underlying.The rat model of MI was successfully established in-vivo. MiR-548c-3p was upregulated via

Comparison of cardioprotective effects using salvianolic acid B and benazepril for the treatment of chronic myocardial infarction in rats.

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The aim of this study was to compare the cardioprotective effects of salvianolic acid B (Sal B) and the angiotension-converting enzyme inhibitor, benazepril, in rats with chronic myocardial infarction (MI) that resulted from a coronary artery ligation for 4 weeks. The rats were divided into four

Increase in the expression of biglycan mRNA expression Co-localized closely with that of type I collagen mRNA in the infarct zone after experimentally-induced myocardial infarction in rats.

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Biglycan, a small dermatan sulphate proteoglycan, has been postulated to interact with other components of the extracellular matrix (ECM), specifically collagens. We hypothesized that biglycan messenger ribonucleic acid (mRNA) is increased in the myocardial infarct zone. Biglycan mRNA expression

Growth hormone attenuates early left ventricular remodeling and improves cardiac function in rats with large myocardial infarction.

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OBJECTIVE We sought to investigate the cardiac effects of growth hormone (GH) administration during the early phase of pathologic remodeling in a rat model of large myocardial infarction (MI). BACKGROUND Recent evidence suggests that exogenous administration of GH evokes a hypertrophic response and

Expression of an endothelial-type nitric oxide synthase isoform in human neutrophils: modification by tumor necrosis factor-alpha and during acute myocardial infarction.

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OBJECTIVE The purpose of this study was to determine whether human neutrophils express an endothelial-type nitric oxide synthase (eNOS), and to study the effect of tumor necrosis factor-alpha (TNF-alpha) on its expression. BACKGROUND Several studies have demonstrated the presence of a constitutively

Active Coxsackieviral B infection is associated with disruption of dystrophin in endomyocardial tissue of patients who died suddenly of acute myocardial infarction.

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OBJECTIVE In this study, we evaluated the potential direct role of enterovirus (EV) cardiac infections in the pathogenesis of myocardial infarction (MI). BACKGROUND Enteroviruses (Picornaviridae) have been suspected to play a role in the development of acute MI. METHODS The presence of EV

MiR-125b Improves acute myocardial infarction in rats by regulating P38/Sirtl/P53 signaling pathway

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The aim of this study was to investigate the differential expression of micro ribonucleic acid (miR)- 125b in acute myocardial infarction (AMI) cases, and to explore the mechanism by which it affects cardiac function. Sprague-Dawley rats were used for AMI modeling, and the expression of miR-125b in

Atrial natriuretic peptide transcription, storage, and release in rats with myocardial infarction.

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To study the role of atrial natriuretic peptide (ANP) in chronic heart failure, ANP synthesis, storage, and release were examined by measuring atrial ANP messenger ribonucleic acid (mRNA) levels and atrial and plasma ANP concentrations in rats with myocardial infarction produced by coronary artery

Downregulated expression of plasminogen activator inhibitor-1 augments myocardial neovascularization and reduces cardiomyocyte apoptosis after acute myocardial infarction.

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OBJECTIVE The aim of this study was to examine whether selective plasminogen activator inhibitor type 1 (PAI-1) downregulation in the acutely ischemic heart increases the myocardial microvasculature and improves cardiomyocyte (CM) survival. BACKGROUND Endogenous myocardial neovascularization is an

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