Planta Med 2004; 70(7): 610-614
DOI: 10.1055/s-2004-827182
Original Paper
Pharmacology
© Georg Thieme Verlag KG Stuttgart · New York

Activation of α1A-Adrenoceptors by Genistein at Concentrations Lower than that to Inhibit Tyrosine Kinase in Cultured C2C12 Cells

Shuo-Bin Jou1 , Ching-Chiu Huang2 , I-Min Liu3 , Juei-Tang Cheng2
  • 1Department of Neurology, School of Medicine and Hospital, China Medical University, Taichung City, Taiwan, R.O.C.
  • 2Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan City, Taiwan, R.O.C.
  • 3Department of Pharmacy, Tajen Institute of Technology, Yen-Pou, Ping Tung Shien, Taiwan, R.O.C.
The present study is supported in part by a grant from National Science Council (NSC-92-2320-B006-003) of the Republic of China
Further Information

Publication History

Received: November 27, 2003

Accepted: March 7, 2004

Publication Date:
15 July 2004 (online)

Abstract

Genistein, an isoflavonoid natural product, is widely used to inhibit protein tyrosine kinase (PTK). In the present study, we investigated the possible influence of genistein on α1-adrenoceptors (AR) in cultured C2C12 cells. Genistein enhanced the uptake of radioactive glucose into C2C12 cells in a concentration-dependent manner. Similar results were also observed in samples treated with daidzein, the inactive congener for PTK inhibition. The effect of genistein on α1-AR was further characterized using the displacement of [3 H]prazosin binding in C2C12 cells. The increase in radioactive glucose uptake by genistein was abolished by RS17053 at a concentration sufficient to block α1A-AR. The pharmacological inhibition of phospholipase C (PLC) by U73122 resulted in a concentration-dependent reduction of genistein-stimulated glucose uptake in C2C12 cells. This inhibition by U73122 was specific because the inactive congener, U73343, failed to modify the action of genistein. Moreover, genistein can activate α1A-AR at a concentration (1 μmol/L) lower than that (50 μmol/L) needed to abolish the insulin-stimulated phosphorylation of PTK. The obtained data indicate an activation of α1A-AR by genistein to increase the glucose uptake into C2C12 cells and this supports the application of genistein as a TK inhibitor.

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Professor Juei-Tang Cheng

Department of Pharmacology

College of Medicine

National Cheng Kung University

Tainan City

Taiwan 70101

R.O.C.

Phone: +886-6-237-2706

Fax: +886-6-238-6548

Email: jtcheng@mail.ncku.edu.tw