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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/108238


    Title: Protective effect of HDL on NADPH oxidase-derived super oxide anion mediates hypoxia-induced cardiomyocyte apoptosis
    Authors: Su-Ying Wen;Shanmugam Ta;Shanmugam Tamilselvi;Chia-Yao She;Chia-Yao Shen;Cecelia Hsua;Cecelia Hsuan Day;Li-Chin Chun;Li-Yi Cheng;Hsiu-Chung O;Hsiu-Chung Ou;Ray-Jade Che;Ray-Jade Chen;Vijaya Padma;Vijaya Padma Viswanadha;Wei-Wen Kuo;黃志揚;Chih-yang Huang
    Contributors: 生物科技學系
    Date: 2017-06
    Issue Date: 2017-10-30 10:45:13 (UTC+8)
    Abstract: Cardiovascular diseases are the leading cause of death of death in Taiwan. Atherosclerosis can lead to serious problems, including heart attack, stroke, or even death. Coronary heart disease (CHD) occurs when plaque builds up in the coronary arteries to cause the ischemic heart disease which will enhance myocardial remodeling and also induce myocardial hypoxia. High density lipoprotein (HDL) has been proposed to have cardio-protective effects. Under hypoxic conditions (1%O2 for 24hr), in H9c2 cells, reactive oxygen species (ROS) is induced which leads to cardiomyocyte apoptosis and cardiac dysfunction. Therefore, the present study described the protective effect of HDL on hypoxia-induced cardiomyocyte damage. We investigated the NADPH oxidase-produced ROS-related signaling pathways and apoptosis in cardiomyocytes under hypoxia conditions. Results showed that the ROS mediated cardiac damage might occur via AT1 and PKC activation. Furthermore, hypoxia downregulated the survival protein (p-AKTser473) and anti-apoptotic protein (BCL2), whereas pro-apoptotic protein, Bax and caspase 3 were upregulated. These detrimental effects by ROS and apoptosis were prevented by HDL pretreatment. Our findings revealed the underlying molecular mechanism by which HDL suppresses the hypoxia-induced cardiomyocyte dysfunction. Further, we elucidated the role of HDL on preventing hypoxia induced cardiomyocyte apoptosis is mediated through the inhibition of NADPH oxidase-derived ROS.
    Relation: PLoS One.
    Appears in Collections:[生物科技學系] 期刊論文

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