Horm Metab Res 2012; 44(01): 33-40
DOI: 10.1055/s-0031-1295416
Original Basic
© Georg Thieme Verlag KG Stuttgart · New York

Antihyperglycemic Effect of Ginsenoside Rh2 by Inducing Islet β-cell Regeneration in Mice

Y. Wang
1   School of Life Science, Sichuan University, Chengdu, Sichuan, China
2   Institute of Organ Transplantation, Sichuan Academy of Medical Science & Sichuan Provincial People’s Hospital, Sichuan, Chengdu, China
,
H. Wang
2   Institute of Organ Transplantation, Sichuan Academy of Medical Science & Sichuan Provincial People’s Hospital, Sichuan, Chengdu, China
,
Y. Liu
3   91388 military hospital, Guangdong, Zhanjiang, China
,
C. Li
1   School of Life Science, Sichuan University, Chengdu, Sichuan, China
,
P. Qi
2   Institute of Organ Transplantation, Sichuan Academy of Medical Science & Sichuan Provincial People’s Hospital, Sichuan, Chengdu, China
,
J. Bao
1   School of Life Science, Sichuan University, Chengdu, Sichuan, China
› Author Affiliations
Further Information

Publication History

received 20 July 2011

accepted 13 October 2011

Publication Date:
28 December 2011 (online)

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Abstract

The present study was designed to determine the antihyperglycemic function of ginsenoside Rh2 (GS-Rh2) by the regeneration of β-cells in mice that underwent 70% partial pancreatectomy (PPx), and to explore the mechanisms of GS-Rh2-induced β-cell proliferation. Adult C57BL/6J mice were subjected to PPx or a sham operation. Within 14 days post-PPx, mice that underwent PPx received GS-Rh2 (1 mg/kg body weight) or saline injection. GS-Rh2-treated mice exhibited an improved glycemia and glucose tolerance, an increased serum insulin levels, and β-cell hyperplasia. Meanwhile, increased β-cell proliferation percentages and decreased β-cell apoptosis percentages were also observed in GS-Rh2-treated mice. Further studies on the Akt/Foxo1/PDX-1 signaling pathway revealed that GS-Rh2 probably induced β-cell proliferation via activation of Akt and PDX-1 and inactivation of Foxo1. Studies on the abundance and activity of cell cycle proteins suggested that GS-Rh2-induced β-cell proliferation may ultimately be achieved through the regulation of cell cycle proteins. These findings demonstrate that GS-Rh2 administration could inhibit the tendency of apoptosis, and reverse the impaired β-cell growth potential by modulating Akt/Foxo1/PDX-1 signaling pathway and regulating cell cycle proteins. Induction of islet β-cell proliferation by GS-Rh2 suggests its therapeutic potential in the treatment of diabetes.