Neuroprotective effects of ginsenoside Rg1 on 1-methyl-4-phenylpyridinum-induced apoptosis in PC12 cells
10.3724/SP.J.1008.2011.00965
- Author:
Xiao-li YE
1
Author Information
1. Department of Cadres
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Cytochromes C;
GinsenosideRg1;
Neuroprotective agents;
PC12 cells
- From:
Academic Journal of Second Military Medical University
2011;32(9):965-968
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the neuroprotective effect of ginsenoside Rg1 against PC12 cell apoptosis induced by 1-methyl-4-phenylpyridinum (MPP++). Methods MPP++-induced apoptosis in PC12 cells, with the characteristics of dopaminergic neuron, were taken as the model of Parkinson disease in vitro. The cells were divided into control group, MPP++ group and 3 ginsenoside Rg1 pretreatment groups (concentrations 10, 20, and 50 μmol/L). MTT assay was used for detecting the cell viability, FCM for apoptosis ratio, TUNEL enzyme labelling for DNA fragment of the cell nuclear, and Western blotting analysis for cytochrome C protein. Results Ginsenoside Rg1 (10, 20, and 50 μmol/L) showed protective effect against MPP++-induced PC12 cells injury. Compared with MPP++-treated cells([52±4.7]%), pretreatment with 10, 20, and 50 μmol/ L ginsenoside Rg1 increased the cell viability to (64 ± 3. 4) %, (72 ± 5.2) % and (83±6.2)%, respectively (P<0.05 or P< 0.01). FCM analysis indicated that apoptosis rates decreased by ginsenoside Rg1 pretreatment, with the apoptosis rates in the control, MPP++ and 3 ginsenoside Rg1 groups (10, 20, 50 μmol/L) being 1.8%, 44.5%, 32.9%, 21.1% and 14.2%, respectively. We also found that ginsenoside Rg1 pretreatment greatly decreased DNA fragment of PC12 cells. Western blotting analysis indicated that the cytochrome C was depressed by the ginsenoside Rg1 pretreatment. Conclusion Ginsenoside Rg1 can protect PC12 cells against MPP++-induced apoptosis in a concentration-dependent manner, which may be closely related to down- regulation of cytochrome C over-expression in the mitochondria.
