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Evidence-Based Complementary and Alternative Medicine
Volume 2014, Article ID 724670, 9 pages
http://dx.doi.org/10.1155/2014/724670
Research Article

Lycopene Inhibits Urotensin-II-Induced Cardiomyocyte Hypertrophy in Neonatal Rat Cardiomyocytes

1Shin Kong Wu Ho-Su Memorial Hospital, Taipei 111, Taiwan
2Department of Surgery, School of Medicine, Taipei Medical University, Taipei 110, Taiwan
3Department of Biological Science and Technology, College of Life Sciences, China Medical University, Taichung 40402, Taiwan
4Division of Cardiology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City 23561, Taiwan
5Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
6Division of Cardiology, Department of Internal Medicine and Graduate Institute of Clinical Medical Science, China Medical University, Taichung 40402, Taiwan
7Institute of Biomedical Sciences, Academia Sinica, Taipei 115, Taiwan
8Department of Biochemistry, School of Medicine, China Medical University, Taichung 40402, Taiwan

Received 3 March 2014; Accepted 24 April 2014; Published 25 May 2014

Academic Editor: Wei-Wen Kuo

Copyright © 2014 Hung-Hsing Chao 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

This study investigated how lycopene affected urotensin-II- (U-II-) induced cardiomyocyte hypertrophy and the possible implicated mechanisms. Neonatal rat cardiomyocytes were exposed to U-II (1 nM) either exclusively or following 6 h of lycopene pretreatment (1–10 μM). The lycopene (3–10 μM) pretreatment significantly inhibited the U-II-induced cardiomyocyte hypertrophy, decreased the production of U-II-induced reactive oxygen species (ROS), and reduced the level of NAD(P)H oxidase-4 expression. Lycopene further inhibited the U-II-induced phosphorylation of the redox-sensitive extracellular signal-regulated kinases. Moreover, lycopene treatment prevented the increase in the phosphorylation of serine-threonine kinase Akt and glycogen synthase kinase-3beta (GSK-3β) caused by U-II without affecting the protein levels of the phosphatase and tensin homolog deleted on chromosome 10 (PTEN). However, lycopene increased the PTEN activity level, suggesting that lycopene prevents ROS-induced PTEN inactivation. These findings imply that lycopene yields antihypertrophic effects that can prevent the activation of the Akt/GSK-3β hypertrophic pathway by modulating PTEN inactivation through U-II treatment. Thus, the data indicate that lycopene prevented U-II-induced cardiomyocyte hypertrophy through a mechanism involving the inhibition of redox signaling. These findings provide novel data regarding the molecular mechanisms by which lycopene regulates cardiomyocyte hypertrophy.