Abstract: Objective To explore the effects of miR- 34a and the alteration of AMPK/mTOR signal pathway on angiotensin (Ang)Ⅱ -stimulated cardiomyocytes hypertrophy. Methods Neonatal rat cardiomyocytes were cultrued in vitro and were divided into 3 groups: negative control for lentivirus carrying miR-34a group (NC), AngⅡ plus lentivirus carrying negative control group (AngⅡ +NC) and AngⅡ plus lentivirus carrying miR-34a group (AngⅡ +miR-34a). The relative cell area was detected by confocal microscopy. The expression of miR-34a and hypertrophy-related genes (ANP and β-MHC) were analyzed by real time PCR. The AMPK/mTOR signal pathway was measured by Western blot assay. Results Compared to NC group, the relative cell area was increased in AngⅡ +NC group (P＜ 0.05). But compared with AngⅡ +NC group, the relative cell area was decreased in AngII+miR- 34a group (P＜ 0.05). Moreover, compared with NC group, the expression of miR- 34a was decreased, and the expression of hyperthophy- related genes(ANP and β- MHC) was upregulated in AngⅡ +NC group. However, the expression of miR- 34a was decreased, and the expression of hyperthophyrelated genes (ANP and β-MHC) was down-regulated (P＜ 0.05). Finally, compared to NC group, the ratio of phosphopAMPK/AMPK was significantly induced in AngII + NC group, but the ratio of phosphop-mTOR/mTOR was significantly decreased (P＜ 0.05). However, compared to Ang Ⅱ + NC group, the ratio of phosphop- AMPK/AMPK was significantly decreased in AngII + miR- 34a group, but the ratio of phosphop- mTOR/mTOR was significantly increased (P＜ 0.05). Conclusion miR-34a is able to inhibit myocardial hypertrophy of neonatal rat cardiomyocytes, and its mechanism is partly carried out by the alteration of the signal pathway of AMPK/mTOR.

Key words: myocytes, cardiac, cardiomyopathy, hypertrophic, angiotensinⅡ , disease models, animal, AMPK/ mTOR, miR-34a