Basic & Clinical Medicine ›› 2014, Vol. 34 ›› Issue (2): 185-189.

Previous Articles     Next Articles

Autophagy inhibitor contributes to apoptosis induced by anoxia in cardiac myocytes


  • Received:2013-04-17 Revised:2013-07-24 Online:2014-02-05 Published:2014-01-13
  • Supported by:
    National Science and Technology Infrastructure Program

Abstract: Objective This study aims to investigate the potential roles of autophagy induced by ischemia in effecting on expression of Bim and caspase-3 and tries to clarify the regulation of HIF-1 in this process. Methods We employed simulated anoxia of neonatal rat ventricular myocytes as an in vitro model of ischemia injury to the heart. Cardiac myocytes were exposed to 0,2,4,8,14 and 24h anoxia. Cardiac myocytes were pretreated with 10mmol/L 3-Methyladenine (3MA) to inhibit autophagy. The beating rate and arrhythm of myocardial cells were detected by inverted microscope. The activity of lactate dehydrogenase was determined by automatic biochemistry analyzer. Western blot analysis was used to examine variation in the expression of LC3-II/I (a marker of autophagy),Bim,caspase-3and HIF-1. Results As the beating rate of myocardial cells was slightly decreased, and the cell arrhythm was increased (P<0.05) after inhibition autophagy; the activity of lactate dehydrogenase was increased (P<0.05)when inhibiting autophagy. Moreover, significant autophagy was reduced by pretreating with 3-Methyladenine (3MA) in anoxia, and the expression of Bim and caspase-3 was significantly increased (P< 0.05). The expression of HIF-1was increased significantly in anoxia group and reduced in anoxia+3MA group (P< 0.05). Conclusion Inhibition of autophagy constitutes a powerful and previously uncharacterized apopotosis induced by anoxia in cardiac myocytes via upregulating the pro-apopototic protein Bim and caspase-3. And HIF-1 positively regulated the process of autophagy induced by anoxia.

Key words: autophagy, anoxia, Bim, caspase-3, HIF-1

CLC Number: