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

• Published in: Bioscience, biotechnology, and biochemistry Vol. 77; no. 2; pp. 229 - 234
• Main Authors: CHANG, Yung-Ming, TSAI, Chuan-Te, WANG, Chiun-Chuang Roger, CHEN, Yueh-Sheng, LIN, Yueh-Min, KUO, Chia-Hua, TZANG, Bor-Show, CHEN, Ray-Jade, TSAI, Fuu-Jen, HUANG, Chih-Yang
• Format: Journal Article
• Language: English
• Published: England Japan Society for Bioscience, Biotechnology, and Agrochemistry 2013
• Subjects: alpinate oxyphyllae fructus; Alpinia - chemistry; angiotensin II; Angiotensin II - pharmacology; Animals; apoptosis; Apoptosis - drug effects; bcl-Associated Death Protein - genetics; bcl-Associated Death Protein - metabolism; Benzimidazoles; Carbocyanines; cardiomyoblast cell; Cardiotonic Agents - isolation & purification; Cardiotonic Agents - pharmacology; Caspase 3 - genetics; Caspase 3 - metabolism; Caspase 9 - genetics; Caspase 9 - metabolism; Cell Line; Cytochromes c - genetics; Cytochromes c - metabolism; Embryo, Mammalian; Fluorescent Dyes; Fruit - chemistry; Gene Expression - drug effects; H9c2 cell; In Situ Nick-End Labeling; Membrane Potential, Mitochondrial - drug effects; Mitochondria - drug effects; Mitochondria - metabolism; Myoblasts, Cardiac - cytology; Myoblasts, Cardiac - drug effects; Myoblasts, Cardiac - metabolism; Plant Extracts - isolation & purification; Plant Extracts - pharmacology; Rats
• ISSN: 0916-8451; 1347-6947
• DOI: 10.1271/bbb.120541

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.