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Abstract
Objective Heart failure and ventricular remodeling after acute myocardial infarction (AMI) are important factors affecting the prognosis of patients. Therefore, we expected to explore the therapeutic target of AMI by studying the effect of death-associated protein kinase 1 (DAPK1) on AMI rat model. Materials and Methods We used male Sprague-Dawley rats to make AMI model, and after 1, 3, 7, and 14 d, we detect the success rate of modeling and the expression change of DAPK1 through 2, 3, 5-triphenyl tetrazolium chloride staining, myocardial injury markers detection, echocardiographic detection, and histological experiment. In addition, we determined the effect of DAPK1 on AMI by subcutaneous injection of the DAPK1 inhibitor (TC-DAPK 6). The effect of DAPK1 on cardiomyocytes has also been verified in cell experiments on H9c2 cells. Results The expression of DAPK1 in AMI rats was significantly higher than that in sham group, and it increased with time. The expression of inflammatory factors (interleukin- (IL-) 1β, IL-6, and tumor necrosis factor-α) in AMI rats treated by TC-DAPK 6 was reduced. In addition, TC-DAPK 6 also reduced the activity of malonaldehyde and increased the activities of superoxide dismutase, glutathione, and catalase. The expression of antioxidant molecules such as peroxiredoxin1/4 and glutathione peroxidase1/3 was also promoted by TC-DAPK 6. In H9c2 cells, TC-DAPK 6 also reduced its oxidative stress level. Conclusions The increase of DAPK1 may be related to the pathogenesis of AMI. DAPK1 inhibitors protect cardiomyocytes from AMI-induced myocardial injury by reducing levels of inflammation and oxidative stress in myocardial tissue and cells.
Highlights
Acute myocardial infarction (AMI) is a cardiovascular disease with high morbidity and high mortality [1]
The loss of myocardial cells after AMI and the subsequent ventricular remodeling are the main causes of a series of complications after AMI, especially heart failure, which affects the prognosis of patients [3]
We found that the scope of myocardial infarction gradually increased with time
Summary
Acute myocardial infarction (AMI) is a cardiovascular disease with high morbidity and high mortality [1]. Current treatment methods include drug thrombolysis, coronary intervention, and coronary artery bypass grafting These treatments have benefited more and more patients, and the mortality rate has decreased significantly, the heart cannot be repaired by the regeneration of myocardial cells due to the poor regeneration of myocardial cells after infarction [2]. How to promote the repair and functional reconstruction of myocardial cells in the necrotic area after AMI and prevent ventricular remodeling has become the key to improving the prognosis of MI patients. Recent studies have found that DAPK1 is an important serine/threonine kinase and is involved in a variety of cell-to-cell interactions, such as apoptosis, autophagy, cellular blebbing, tumor metastasis, and inflammation [5, 6]. In this study, we made the rat AMI model to detect DAPK1 expression changes and used DAPK1 inhibitors to detect their effect on AMI rats and cardiomyocytes
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