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

• Published in: Evidence-based complementary and alternative medicine 2014-01, Vol.2014 (2014), p.1-9
• Main Authors: Chen, Jin-Jer, Liu, Ju-Chi, Chen, Cheng-Hsien, Sung, Li-Chin, Chao, Hung-Hsing, Cheng, Tzu-Hurng
• Format: Article
• Language: English
• Subjects: AKT protein; Cardiomyocytes; Cardiovascular disease; Carotenoids; Cell cycle; Chromosome 10; Glycogen; Glycogen synthase kinase 3; Heart; Homology; Hypertrophy; Inactivation; Kinases; Laboratory animals; Lycopene; Molecular chains; Molecular modelling; NAD; NAD(P)H oxidase; Neonates; Newborn babies; Oxidative stress; Phosphorylation; Protein-serine/threonine kinase; PTEN protein; Reactive oxygen species; Rodents; Tensin
• ISSN: 1741-427X; 1741-4288
• DOI: 10.1155/2014/724670

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.