eCAM Advance Access originally published online on June 20, 2006
eCAM 2006 3(3):365-372; doi:10.1093/ecam/nel026
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© 2006 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commerical use, distribution, and reproduction in any medium, provided the original work is properly cited.
American Ginseng Stimulates Insulin Production and Prevents Apoptosis through Regulation of Uncoupling Protein-2 in Cultured ß Cells
1 PLME Department of Medicine, Brown University Providence, RI 02912, USA, and 2 The Center for Stem Cell Biology, Department of Research, Roger Williams Hospital Providence, RI 02908, USA
American ginseng root displays the ability to achieve glucose homeostasis both experimentally and clinically but the unknown mechanism used by ginseng to achieve its therapeutic effects on diabetes limits its application. Disruption in the insulin secretion of pancreatic ß cells is considered the major cause of diabetes. A mitochondrial protein, uncoupling protein-2 (UCP-2) has been found to play a critical role in insulin synthesis and ß cell survival. Our preliminary studies found that the extracts of American ginseng inhibit UCP-2 expression which may contribute to the ability of ginseng protecting ß cell death and improving insulin synthesis. Therefore, we hypothesized that ginseng extracts suppress UCP-2 in the mitochondria of pancreatic ß cells, promoting insulin synthesis and anti-apoptosis (a programmed cell-death mechanism). To test the hypothesis, the serum-deprived quiescent ß cells were cultured with or without interleukin-1ß (IL-1ß), (200 pg ml–1, a cytokine to induce ß cell apoptosis) and water extracts of American ginseng (25 µg per 5 µl administered to wells of 0.5 ml culture) for 24 h. We evaluated effects of ginseng on UCP-2 expression, insulin production, anti-/pro-apoptotic factors Bcl-2/caspase-9 expression and cellular ATP levels. We found that ginseng suppresses UCP-2, down-regulates caspase-9 while increasing ATP and insulin production/secretion and up-regulates Bcl-2, reducing apoptosis. These findings suggest that stimulation of insulin production and prevention of ß cell loss by American ginseng extracts can occur via the inhibition of mitochondrial UCP-2, resulting in increase in the ATP level and the anti-apoptotic factor Bcl-2, while down-regulation of pro-apoptotic factor caspase-9 occurs, lowering the occurrence of apoptosis, which support the hypothesis.
Keywords: American ginseng – apoptosis – ATP – ß cell – Bcl-2 – caspase – insulin – mitochondria – UCP-2
For reprints and all correspondence: Dr Luguang Luo, The Center for Stem Cell Biology, Department of Research, Roger Williams Hospital, 825 Chalkstone Avenue, Providence, RI 02908. Tel: +1-401-456-5344; Fax: +1-401-456-5759; E-mail: Lluo{at}rwmc.org
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