Fruit-juice concentrate of Asian plum inhibits growth signals of vascular smooth muscle cells induced by angiotensin II

Bainiku-ekisu, the fruit-juice concentrate of the Oriental plum ( Prunus mume) has recently been shown to improve human blood fluidity. We have shown that angiotensin II (AngII) stimulates growth of vascular smooth muscle cells (VSMCs) through epidermal growth factor (EGF) receptor transactivation t...

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Published in:Life sciences (1973) Vol. 72; no. 6; pp. 659 - 667
Main Authors: Utsunomiya, Hirotoshi, Takekoshi, Susumu, Gato, Nobuki, Utatsu, Hisao, Motley, Evangeline D, Eguchi, Kunie, Fitzgerald, Trinita G, Mifune, Mizuo, Frank, Gerald D, Eguchi, Satoru
Format: Journal Article
Language:English
Published: Netherlands Elsevier Inc 27-12-2002
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Summary:Bainiku-ekisu, the fruit-juice concentrate of the Oriental plum ( Prunus mume) has recently been shown to improve human blood fluidity. We have shown that angiotensin II (AngII) stimulates growth of vascular smooth muscle cells (VSMCs) through epidermal growth factor (EGF) receptor transactivation that involves reactive oxygen species (ROS) production. To better understanding the possible cardiovascular protective effect of Bainiku-ekisu, we have studied whether Bainiku-ekisu inhibits AngII-induced growth promoting signals in VSMCs. Bainiku-ekisu markedly inhibited AngII-induced EGF receptor transactivation. H 2O 2-induced EGF receptor transactivation was also inhibited by Bainiku-ekisu. Thus, Bainiku-ekisu markedly inhibited AngII-induced extracellular signal-regulated kinase (ERK) activation. However, EGF-induced ERK activation was not affected by Bainiku-ekisu. AngII stimulated leucine uptake in VSMCs that was significantly inhibited by Bainiku-ekisu. Also, Bainiku-ekisu possesses a potent antioxidant activity. Since the activation of EGF receptor, ERK and the production of ROS play central roles in mediating AngII-induced vascular remodeling, these data suggest that Bainiku-ekisu could exert a powerful cardiovascular protective effect with regard to cardiovascular diseases.
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ISSN:0024-3205
1879-0631
DOI:10.1016/S0024-3205(02)02300-7