Alpinate Oxyphyllae Fructus (Alpinia Oxyphylla Miq) Extracts Inhibit Angiotensin-II Induced Cardiac Apoptosis in H9c2 Cardiomyoblast Cells

DOI Web Site PubMed 参考文献73件
  • CHANG Yung-Ming
    Department of Chinese Medicine, China Medical University Hospital School of Chinese Medicine, China Medical University
  • TSAI Chuan-Te
    1PT Biotechnology Co., Ltd.
  • WANG Chiun-Chuang Roger
    Department of Food and Nutrition, Providence University
  • CHEN Yueh-Sheng
    School of Chinese Medicine, China Medical University
  • LIN Yueh-Min
    Department of Pathology, Changhua Christian Hospital Department of Medical Technology, Jen-Teh Junior College of Medicine, Nursing, and Management
  • KUO Chia-Hua
    Laboratory of Exercise Biochemistry, Taipei Physical Education College
  • TZANG Bor-Show
    Institute of Biochemistry and Biotechnology, Chung Shan Medical University
  • CHEN Ray-Jade
    Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University
  • TSAI Fuu-Jen
    School of Chinese Medicine, China Medical University
  • HUANG Chih-Yang
    Graduate Institute of Basic Medical Science, China Medical University Department of Health and Nutrition Biotechnology, Asia University

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Angiotensin II (Ang II) is a risk factor for cardiovascular disease. We used a traditional Chinese medicine, alpinate oxyphyllae fructus (AOF), to evaluate its effect on Ang II-induced cardiac apoptosis and mitochondrial dysfunction. Ang II-treated H9c2 cells were administered AOF of 20–100 µg/mL concentrations. Ang II significantly increased TUNEL-positive nuclei in the H9c2 cells, effect was inhibited by AOF administration in both pre-treated and post-treated H9c2 cells. Caspases 9 and 3 activities were increased by Ang II and downregulated by AOF administration, especially in pre-treatment. AOF treatment reversed Ang II-induced mitochondria membrane potential instability in H9c2 cells as observed by JC-1 stain assay. Furthermore, pro-apoptotic proteins Bad and cytochrome c increased and decreased respectively under AOF administration. The levels of p-Bad anti-apoptotic protein were significantly increased after AOF treatment. This study indicates that mitochondrial dependent apoptosis induced by Ang II.

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