Role of CAPE on cardiomyocyte protection via connexin 43 regulation under hypoxia

Int J Med Sci. 2016 Sep 20;13(10):754-758. doi: 10.7150/ijms.15847. eCollection 2016.


Background: Cardiomyocyte under hypoxia cause cell death or damage is associated with heart failure. Gap junction, such as connexin 43 play a role in regulation of heart function under hypoxia. Caffeic acid phenethyl ester (CAPE) has been reported as an active component of propolis, has antioxidative, anti-inflammatory antiproliferative and antineoplastic biological properties. Aims: Connexin 43 appear to have a critical role in heart failure under hypoxia, there has been considerable interest in identifying the candidate component or compound to reduce cell death. Methods: In this study, we used human cardiomyocyte as a cell model to study the role of connexin 43 in hypoxia- incubated human cardiomyocyte in absence or presence of CAPE treatment. Results: Results showed that hypoxia induced connexin 43 expression, but not altered in connexin 40. Interestingly, CAPE attenuates hypoxia-caused connexin 43 down-regulation and cell death or cell growth inhibition. Conclusion: We suggested that reduction of cell death in cardiomyocytes by CAPE is associated with an increase in connexin 43 expression.

Keywords: Caffeic acid phenethyl ester (CAPE); cardiomyocyte; connexin 43.; hypoxia.

MeSH terms

  • Caffeic Acids / metabolism*
  • Cell Line
  • Connexin 43 / metabolism*
  • Humans
  • Hypoxia / metabolism*
  • L-Lactate Dehydrogenase / metabolism
  • Mitochondria, Heart / metabolism*
  • Myocardial Ischemia / metabolism
  • Myocytes, Cardiac / metabolism*
  • Phenylethyl Alcohol / analogs & derivatives*
  • Phenylethyl Alcohol / metabolism


  • Caffeic Acids
  • Connexin 43
  • GJA1 protein, human
  • L-Lactate Dehydrogenase
  • caffeic acid phenethyl ester
  • Phenylethyl Alcohol