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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.

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