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

Research Paper

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

Chien-Cheng Chen1*, Chan-Yen Kuo2*, Rong-Fu Chen3✉

1. Department of Cardiology, Show Chwan Memorial Hospital, Changhua, Taiwan.
2. Graduate Institute of Systems Biology and Bioinformatics, National Central University, Chung-li, Taiwan, 32001, Republic of China.
3. Research Assistant Center, Show Chwan Health Care System, Changhua, Taiwan.
*These two authors equally contribute to this study.


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, hypoxia, connexin 43.

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How to cite this article:
Chen CC, Kuo CY, Chen RF. Role of CAPE on cardiomyocyte protection via connexin 43 regulation under hypoxia. Int J Med Sci 2016; 13(10):754-758. doi:10.7150/ijms.15847. Available from