American Journal of Pharmacy and Pharmacology 2016; 3(1): 1-5 Published online February 16, 2016 (http://www.aascit.org/journal/ajpp) ISSN: 2375-3900 Keywords Caffeic Acid Phenethyl Ester (CAPE), Cardiomyocyte, Hypoxia Received: January 7, 2016 Revised: January 14, 2016 Accepted: January 16, 2016 Caffeic Acid Phenethyl Ester (CAPE) Reduces LDH Release and Cell Cytotoxicity in Cardiomyocyte Huan-Nung Chao 1 , Chia-Hsing Leu 2 , Chien-Cheng Chen 1 , Chun-Yen Huang 3 , Chan-Yen Kuo 2, * 1 Division of Cardiology, Show Chwan Memoialy Hospital, Changhua, Taiwan, Republic of China 2 Graduate Institute of Systems Biology and Bioinformatics, National Central University, Chung-li, Taiwan, Republic of China 3 Medical Research Department, E-Da Hospital, Kaohsiung City, Taiwan, Republic of China Email address cykuo@thu.edu.tw (Chan-Yen Kuo) Citation Huan-Nung Chao, Chia-Hsing Leu, Chien-Cheng Chen, Chun-Yen Huang, Chan-Yen Kuo. Caffeic Acid Phenethyl Ester (CAPE) Reduces LDH Release and Cell Cytotoxicity in Cardiomyocyte. American Journal of Pharmacy and Pharmacology. Vol. 3, No. 1, 2016, pp. 1-5. Abstract Background: Ischemia cardiomyocyte undergo death or damage has been identified as essential process in the progression of heart failure. Under hypoxic conditions, mitochondria can represent a threat to the cell because of their capacity to generate toxic reactive oxygen species (ROS). Aims: As ROS appear to have a critical role in heart failure, there has been considerable interest in identifying the candidate component or compound to reduce cell death via oxidative stress inhibition. Methods: In this study, we used human cardiomyocyte and embryonic rat heart derived H9c2 cells as cell models to speculate the role of ROS in cardiomyocytes. Results: Results showed that hypoxia or hydrogen peroxide (H 2 O 2 ) induced cells Lactate dehydrogenase (LDH) release and cytotoxicity. Interestingly, caffeic acid phenethyl ester (CAPE) reverses hypoxia-induced LDH release and cell death in human cardiomyocyte, as well as ROS scavenger, Tiron also prevents H 2 O 2 induces LDH release and cytotoxicity. Conclusion: Results demonstrate that reduction of cell death in cardiomyocytes by CAPE is associated with a decrease in cellular LDH level and ROS production. 1. Introduction Coronary artery disease (CAD) are major diseases causing heavy burden of many countries and people around the world [1]. It has been reported that the atherosclerosis, the main cause of CAD, is involved in endothelial dysfunction and inflammation [2-4]. Furthermore, Lavie et al. reported that exercise is a secondary prevention of CAD [5], and some reports indicated that exercise seems to be improved the endothelial function [6, 7]. Nitric oxide (NO) plays a critical role in regulation of endothelial function. Production of NO is either increased by endothelial nitric oxide synthase (eNOS) enzymes [8-10] or reduced by reactive oxygen species (ROS) [11]. ROS production is increased in mitochondria upon hypoxia, as well as, ischemic preconditioning (IPC) [12, 13]. Additionally, hypoxia-inducible factor transcription factors (HIF) is upregulated upon hypoxia [14], and triggers the expression of genes involved in oxygen transport, glycolytic metabolism, cell death, cell survival, and other processes that can affect cell survival in ischemia [13]. Caffeic acid phenethyl ester (CAPE) is the major active element of propolis and has an anti- proliferative effect on tumor cells [15, 16]. The antioxidative