| Abstract: | Objective: To explore the effect and mechanism of microRNA-208a(mi R-208a) in the mitochondrial apoptosis of cardiomyocytes of neonatal rats. Methods: The primary cultured cardiomyocytes of neonatal rats were added into the hypoxia incubator for the hypoxia induction. The overexpression system for mi R-208 a of cardiomyocytes of neonatal rats was built. The l ow cytometry assay was employed to detect the incidence of apoptosis in the overexpressed mi R-208 a. The mitochondrial staining technique was used to detect the change in the mitochondrial morphology of over-expressed mi R-208 a. The bioinformatic analysis was chosen to analyze and predict the target gene of mi R-208 a. Results: Firstly, the primary culture system of cardiomyocytes of neonatal rats was successfully built. The mi R-208 a was over-expressed in cardiomyocytes of neonatal rats by mi R-208 a Mimics. Results of flow cytometry assay showed that the over-expressed mi R-208 a could signii cantly reduce the incidence of apoptosis; while results of mitochondrial staining indicated the change in the mitochondrial morphology of over-expressed mi R-208 a and the mitochondrialfission process was inhibited. In conclusion, it was supposed that mi R-208 a could inhibit the activation of mitochondrialfission process to keep the cardiomyocytes from apoptosis. Conclusions: The over-expressed mi R-208 a can reduce the incidence of apoptosis in the cardiomyocytes of neonatal rats, signii cantly change the mitochondrial morphology and inhibit the mitochondrial fission process. |
