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An ethyl acetate extract from a subaleurone layer of Japanese rice inhibits angiotensin ll–induced signal transduction and hypertrophy in vascular smooth muscle cells
Author(s) -
Takaguri Akira,
Utsnomiya Hirotoshi,
Kono Ryohei,
Akazawa Shinichi,
Eguchi Satoru
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.603.4
Subject(s) - vascular smooth muscle , signal transduction , angiotensin ii , ethyl acetate , phosphorylation , chemistry , endocrinology , medicine , muscle hypertrophy , microbiology and biotechnology , pharmacology , biochemistry , receptor , biology , smooth muscle
Objective Rice has been consumed well in many countries. However, whether rice contains an ingredient useful to prevent cardiovascular diseases remains unknown. We have shown that angiotensin II (AngII) induces hypertrophy and migration of vascular smooth muscle cells (VSMCs) through activation of epidermal growth factor receptor (EGFR) and Rho/Rho‐kinase. A subaleurone layer of rice is rich in oligosaccharide and dietary fibers. In this study, we examined the effects of ethyl acetate extract from a subaleurone layer on AngII‐induced signal transduction and hypertrophy in VSMCs. Methods and Results VSMCs were prepared from the aorta of 12‐week‐old male Sprague Dawley rats. Phosphorylation and expression of the signaling proteins were evaluated by immuoblotting. Pretreatment of the ethyl acetate extract (100 μg/ml) inhibited AngII (100 nM)‐induced EGFR transactivation and phosphorylation of a ROCK substrate, myosin phosphatase target subunit‐1. Also, AngII‐induced c‐fos expression was inhibited by the ethyl acetate extract. Thus, AngII‐induced hypertrophy was significantly inhibited by the ethyl acetate extract. Conclusion These data suggest that an ethyl acetate extract from a subaleurone layer might have a protective effect toward cardiovascular diseases by interfering with signal transduction induced by enhanced rennin‐angiotensin system