Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/30909
Title: Ginsenoside Rg1 protects against 6-OHDA-induced toxicity in MES23.5 cells via Akt and ERK signaling pathways
Authors: Ge, KL
Chen, WF
Xie, JX
Wong, MS 
Keywords: 6-OHDA
Akt
ERK
Ginsenoside Rg1
MES23.5 cells
Issue Date: 2010
Publisher: Elsevier
Source: Journal of ethnopharmacology, 2010, v. 127, no. 1, p. 118-123 How to cite?
Journal: Journal of ethnopharmacology 
Abstract: Aim of the study: The present study was designed to investigate the neuroprotective effects of ginsenoside Rg1 against 6-hydroxydopamine (6-OHDA)-induced toxicity in MES23.5 cells and their possible mechanisms. Materials and methods: MES23.5 cells were treated with or without Rg1 for 24 h before exposure to 6-OHDA. Cell viability was determined by MTS assay. The gene and protein expressions of Bcl-2 were detected by real time RT-PCR and western blotting. Phosphorylation of Akt and ERK1/2 were examined by western blotting. Results: Pretreatment with ginsenoside Rg1 had obvious neuroprotective effects on cell viability against 6-OHDA-induced toxicity. 6-OHDA decreased the gene and protein expressions of Bcl-2. These effects could be reversed by Rg1 pretreatment. Potential cell signaling candidates involved in this neuroprotective effect were examined. 6-OHDA significantly inhibited the phosphorylation of Akt and increased the phosphorylation of ERK1/2 in MES23.5 cells. Pretreatment with ginsenoside Rg1 could increase the Akt phosphorylation and inhibit the ERK1/2 phosphorylation induced by 6-OHDA. Further study revealed that LY294002, an inhibitor of phosphatidylinositol 3-kinase (PI3-K), attenuated the neuroprotective effect of Rg1 on cell viability against 6-OHDA-induced toxicity. Conclusions: Taken together, our results strongly suggest that ginsenoside Rg1 has neuroprotective effects against 6-OHDA-induced toxicity in MES23.5 cells. Its mechanism includes the up-regulation of Bcl-2 gene expression, the activation of Akt phoshphorylation as well as the inhibition of ERK1/2 phosphorylation induced by 6-OHDA.
URI: http://hdl.handle.net/10397/30909
ISSN: 0378-8741
EISSN: 1872-7573
DOI: 10.1016/j.jep.2009.09.038
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