Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/14215
Title: Involvement of IGF-I receptor and estrogen receptor pathways in the protective effects of ginsenoside Rg1 against A beta(25-35)-induced toxicity in PC12 cells
Authors: Chen, WF
Zhou, LP
Chen, L
Wu, L
Gao, QG
Wong, MS 
Keywords: Ginsenoside Rg1
Beta-Amyloid peptide
Estrogen receptor
Insulin-like growth factor-I receptor
PC12 cells
Issue Date: 2013
Publisher: Pergamon-Elsevier Science Ltd
Source: Neurochemistry international, 2013, v. 62, no. 8, p. 1065-1071 How to cite?
Journal: Neurochemistry International 
Abstract: Ginsenoside Rg1 is the main pharmacologically active compound of ginsenosides and has demonstrated pharmacological effects in the cardiovascular system, central nervous system and immune system. The involvement of insulin-like growth factor-I receptor (IGF-IR)-dependent pathway and estrogen receptor (ER)-dependent pathway in the biological effect of ginsenoside Rg1 have been demonstrated in our previous study. The present study tested the hypothesis that the protective effects of Rg1 against A beta(25-35)-induced toxicity involved activation of the IGF-IR and ER signaling pathways in PC12 cells. Treatment with A beta(25-35) decreased the cell viability in a dose-dependent manner in PC12 cells. Rg1 pretreatment resulted in an enhancement of survival and the maximum protection occurred at the concentration of 1 mu M. Co-treatment with IGF-IR antagonist JB-1 or ER antagonist ICI182,780 could completely block the protective effect of Rg1. The decreased Bcl-2 mRNA expression induced by A beta(25-35) could be restored by Rg1 pretreatment. Rg1 pretreatment could also restore the decreased mitochondrial membrane potential induced by A beta(25-35) and these effects could be completely blocked by JB-1 or ICI182,780. In addition, Rg1 treatment alone could significantly increase the phosphorylation level of MEK and ERK in a time-dependent manner and the functional transactivation of ER alpha in PC12 cells. The functional transactivation of ER alpha by Rg1 could be completely blocked by JB-1 or ICI182,780. Taken together, our results suggest that IGF-IR and ER signaling pathways might be involved in the protective effect of Rg1 against A beta(25-35)-induced toxicity in PC12 cells.
URI: http://hdl.handle.net/10397/14215
ISSN: 0197-0186
DOI: 10.1016/j.neuint.2013.03.018
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