This study aimed to explore the function of miR-24 in hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury. We constructed a cardiomyocyte model of H/R using the primary cardiomyocytes isolated from Sprague-Dawley rats. To explore the role of miR-24, cells were transfected with a miR-24 mimic or miR-24 inhibitor. The RNA expression levels of miR-24 and Mapk14 were determined using qRT-PCR. The proliferation and apoptosis of cells were determined using a CCK8 assay and a flow cytometer. The TargetScan website was used to predict the targets of miR-24. A dual-luciferase reporter gene assay was conducted to verify whether Mapk14 is indeed a target of miR-24. A Western blot was applied for protein detection. H/R exposure decreased the expression of miR-24 in rat cardiomyocytes. Transfection of the miR-24 mimic into cardiomyocytes reduced H/R-induced injury as evidenced by an increase in proliferation and a decrease in the apoptotic rate. By contrast, transfection of the miR-24 inhibitor aggravated H/R-induced injury. The expression of Bcl-2 was increased while the levels of Bax and Active-caspase 3 were reduced in the H/R+ miR-24 mimic group compared to those in the H/R group. H/R+miR-24 inhibitor group showed the opposite results. Mapk14 was identified as a target of miR-24. The mRNA level of Mapk14 and its protein (p38 MAPK) level were negatively affected by miR-24. Furthermore, we discovered that depletion of Mapk14 reduced the promoting effect of the miR-24 inhibitor on cell apoptosis. Overall, our results illustrated that miR-24 could attenuate H/R-induced injury partly by regulating Mapk14.

Objective. To observe the efficacy and safety of dopamine plus furosemide in treating patients with heart failure. Methods. This research included 150 patients with heart failure who were diagnosed and treated at our hospital between March 2018 and November 2020. The patients were randomly assigned to a study group or a reference group according to the data of admission (the cut-off date was June 2019). Patients in the reference group were given furosemide, whereas those in the study group were given dopamine plus furosemide intravenous pumping. Outcome measures included clinical effectiveness, heart function changes, and adverse responses. Results. Dopamine plus furosemide resulted in higher treatment efficiency (96.00%) versus furosemide (74.67%) study group ( P < 0.05 ). Before therapy, there was no significant change in the scores of cardiac function indices between the two groups ( P > 0.05 ). The cardiac function of the two groups of patients was improved after treatment, and the left ventricular ejection fraction (LVEF) of the study group (44.85 ± 4.12) was higher than that of the reference group (38.45 ± 4.36), and the left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter (LVESD), and plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) (43.17 ± 3.98, 51.32 ± 4.25, 3045.56 ± 365.48) were lower than the reference group (47.56 ± 4.65, 56.28 ± 4.85, 4856.48 ± 395.46) ( P < 0.05 ). There was no significant difference in the total incidence of adverse reactions between the two groups ( P > 0.05 ). Conclusion. Dopamine plus intravenous furosemide infusion treatment has an obvious therapeutic benefit in treating patients with heart failure and dramatically enhances cardiac function without noteworthy adverse responses. It demonstrated great potential for clinical promotion.

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