Chinese Journal Of Clinical Anatomy ›› 2018, Vol. 36 ›› Issue (4): 419-422.doi: 10.13418/j.issn.1001-165x.2018.04.013

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The regulation of hypoxic induced factor on autophagy of myocardial cells in oxygen-glucose deprivation model

SONG Hai-yan, LIAN Hui, ZHANG Yi-min, FU Sheng-qi   

  1. Department of Anatomy, Xinxiang Medical University,Xinxiang 453003, Henan  Province, China; Key Laboratory for Medical Tissue Regeneration of Henan Province, Xinxiang 453003,  Henan Province, China;Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine,Xinxiang 453003, Henan Province, China
  • Received:2017-12-26 Online:2018-07-25 Published:2018-08-21

Abstract:

Objective To investigate the effect of HIF-1α on autophage-associated genes Beclin1, LC3I and LC3II, and the regulation on autophagy.   Methods The model of oxygen-glucose deprivation (OGD) was established, and western blot was used to detect interference effect of HIF-1α siRNA. The CCK-8 assay was used to detect the effect of HIF-1α siRNA on the activity of myocardial cells in OGD model. The effect of HIF-1α siRNA on autophagy-associated genes Beclin1, LC3I and LC3II expression was detected by RT-qPCR and western blot.    Results   The results of western blot showed that HIF-1α siRNA could effectively knock down the expression of HIF-1α in myocardial cells in OGD model. The result of CCK-8 assay showed that HIF-1α siRNA could reduce the activity of myocardial cells in OGD model. RT-qPCR and western blot results showed that HIF-1α siRNA could reduce the expression of the autophagy-associated genes Beclin1, LC3I and LC3II, and reduce the ratio of LC3II to LC3I at mRNA and protein level.  Conclusion    HIF-1α siRNA could knock down the expression of HIF-1α in the OGD model, resulting in further decrease of the activity of myocardial cells,with the Beclin1 expression and ratio of LC3II/LC3I reduced. HIF-1α plays a role of myocardial protection in the OGD model by regulation of autophagy.

Key words:  Ischemia,  Hypoxia,  Autophagy; Hypoxic induction factor,  Myocardial injury