动物造模,心肌肥大 z-bio 2022-11-24 274

　　Objective: To study the mechanism of miR-133a on myocardial hypertrophy in vitro.

　　Methods: The miR-133a adenovirus expression vector was constructed, and was introduced into 293 cells; Cardiac myocytes were obtained from 12 mouse hearts born within 1-3 days by enzyme digestion and gradient centrifugation, and were divided into control group and model group. The model group was induced by phenylephrine (PE); Myocardial cells of the adenovirus infected model group with high expression of miR-133a were used to observe the change of cell area. The expression of Acta1, Actc1, Actb, Myh6, Myh7 and BNP genes were detected by RT-PCR.

　　Results: Compared with the control group, the area of myocardial cells in the model group was more than 3 times larger and the expression of Acta1 and other genes was significantly increased after the model group was cultured with PE; Compared with the model group without miR-133a virus, the area of myocardial cells in the hypertrophic model group infected with miR-133a virus decreased, and the expression of Acta1 and other genes decreased significantly.

　　Conclusion: miR-133a is an important regulator of cardiac hypertrophy and has the effect of antagonizing cardiac hypertrophy.