Chia Nan University of Pharmacy & Science Institutional Repository:Item 310902800/31763
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    標題: Protective effect of HDL on NADPH oxidase-derived super oxide anion mediates hypoxia-induced cardiomyocyte apoptosis
    作者: Wen, Su-Ying
    Tamilselvi, Shanmugam
    Shen, Chia-Yao
    Day, Cecilia Hsuan
    Chun, Li-Chin
    Cheng, Li-Yi
    Ou, Hsiu-Chung
    Chen, Ray-Jade
    Viswanadha, Vijaya Padma
    Kuo, Wei-Wen
    Huang, Chih-Yang
    貢獻者: Taipei City Hosp, Renai Branch, Dept Dermatol
    Mackay Jr Coll Med Nursing & Management, Ctr Gen Educ
    China Med Univ, Grad Inst Basic Med Sci
    MeiHo Univ, Dept Nursing
    Chia Nan Univ Pharm & Sci, Dept Hosp & Hlth Care Adm
    Asia Univ, Dept Biol Sci & Technol
    Taipei Med Univ, Dept Surg, Sch Med, Coll Med
    Bharathiar Univ, Dept Biotechnol, Coimbatore
    China Med Univ, Dept Biol Sci & Technol
    China Med Univ, Grad Inst Chinese Med Sci
    關鍵字: Serum Response Factor
    N-Terminal Kinases
    Neutrophil Respiratory Burst
    Activated Protein-Kinases
    Oxidative Stress
    Heart-Failure
    Cardiovascular-Disease
    Gene-Expression
    Hif-1-Alpha
    Angiogenesis
    日期: 2017-06-15
    上傳時間: 2018-11-30 15:55:47 (UTC+8)
    出版者: Public Library Science
    摘要: 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%O-2 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-AKT(ser473)) 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.
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