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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. |
| 關聯: | Plos One, v.12, n.6, e0179492 |
| 顯示於類別: | [醫務管理系(所)] 期刊論文
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