Neuroprotective effects of ginsenoside Rgl on l-methyl-4-phenylpyridinum-induced apoptosis in PC12 cells / 第二军医大学学报

ABSTRACT

Objective To explore the neuroprotective effect of ginsenoside Rg1 against PC12 cell apoptosis inducedby 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 |imol/ 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.