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Vol.3 , No. 1, Publication Date: Feb. 18, 2016, Page: 1-5
 Reduces LDH Release and Cell Cytotoxicity in Cardiomyocyte&description=<i>Background:</i> 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). <i>Aims:</i> 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. <i>Methods:</i> 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. <i>Results:</i> Results showed that hypoxia or hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) 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<sub>2</sub>O<sub>2</sub> induces LDH release and cytotoxicity. <i>Conclusion:</i> Results demonstrate that reduction of cell death in cardiomyocytes by CAPE is associated with a decrease in cellular LDH level and ROS production.&picture=http://www.aascit.org/aascit/decorators/img/journal/922.jpg)
| [1] | Huan-Nung Chao, Division of Cardiology, Show Chwan Memoialy Hospital, Changhua, Taiwan, Republic of China. |
| [2] | Chia-Hsing Leu, Graduate Institute of Systems Biology and Bioinformatics, National Central University, Chung-li, Taiwan, Republic of China. |
| [3] | Chien-Cheng Chen, Division of Cardiology, Show Chwan Memoialy Hospital, Changhua, Taiwan, Republic of China. |
| [4] | Chun-Yen Huang, Medical Research Department, E-Da Hospital, Kaohsiung City, Taiwan, Republic of China. |
| [5] | Chan-Yen Kuo, Graduate Institute of Systems Biology and Bioinformatics, National Central University, Chung-li, Taiwan, Republic of China. |
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 (H2O2) 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 H2O2 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.
Keywords
Caffeic Acid Phenethyl Ester (CAPE), Cardiomyocyte, Hypoxia
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