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BioMed Research International
Volume 2014 (2014), Article ID 723084, 9 pages
http://dx.doi.org/10.1155/2014/723084
Research Article

Ginseng Is Useful to Enhance Cardiac Contractility in Animals

1Department of Neurosurgery, Taipei Medical University-Shuang Ho Hospital and College of Medicine, Taipei Medical University, Taipei 10361, Taiwan
2Department of Anesthesiology, Taipei Medical University-Shuang Ho Hospital and College of Medicine, Taipei Medical University, Taipei 10361, Taiwan
3Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan
4Department of Nursing, Tzu Chi College of Technology, Hualien City 97005, Taiwan

Received 7 December 2013; Accepted 25 December 2013; Published 4 February 2014

Academic Editor: Juei-Tang Cheng

Copyright © 2014 Jia-Wei Lin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Ginseng has been shown to be effective on cardiac dysfunction. Recent evidence has highlighted the mediation of peroxisome proliferator-activated receptors (PPARs) in cardiac function. Thus, we are interested to investigate the role of PPARδ in ginseng-induced modification of cardiac contractility. The isolated hearts in Langendorff apparatus and hemodynamic analysis in catheterized rats were applied to measure the actions of ginseng ex vivo and in vivo. In normal rats, ginseng enhanced cardiac contractility and hemodynamic significantly. Both actions were diminished by GSK0660 at a dose enough to block PPARδ. However, ginseng failed to modify heart rate at the same dose, although it did produce a mild increase in blood pressure. Data of intracellular calcium level and Western blotting analysis showed that both the PPARδ expression and troponin I phosphorylation were raised by ginseng in neonatal rat cardiomyocyte. Thus, we suggest that ginseng could enhance cardiac contractility through increased PPARδ expression in cardiac cells.