[Ginsenoside-Rg1 inhibits cell apoptosis induced by beta amyloid].
OBJECTIVE
To investigate the effects of ginsenoside-Rg1 on the apoptosis induced by beta amyloid (Abeta) and mechanism thereof so as to search an approach to prevent and treat Alzheimer' s disease.


METHODS
(1) Chinese hamster ovarian tumor cells of the line CHO unable to produce endogenous Abeta were cultured and randomly divided into 3 group: control group, Abeta25-35 group treated with Abeta25-35, and ginsenoside-Rg1 and Abeta25-35 group treated with ginsenoside-Rg1 of the concentrations of 10, 12.5, 25, 50, and 100 micromol/L respectively for 12 h and then treated with Abeta25-35. MTT method was used to dete4ct the survival rate of the CHO cells. (2) Chinese hamster ovarian tumor CHO cells transfected with mutant PSIM146L gene and wild type APP751 gene (mutant PSM146L/APP751 cells) stably producing excessive Abeta1-42 and wild type PSI cells were randomly divided into groups added with ginsenoside-Rg1 of the concentration of 25 micromol/L and groups without ginsenoside-Rg1. Annexin V-FITC/PI apoptosis kit and TUNEL kit were used to detect the apoptotic cells. Immunofluorescence staining was used to detect the protein expression levels of and caspase-3 that mediates the cell apoptosis induced by Abeta. Western blotting was used to detect the protein expression of caspase-3.


RESULTS
Ginsenoside-Rg1 25, 5, and 100 micromol/L dose-dependently increased the cytoactivity level of the CHO cells (all P < 0.05) compared with that of the untreated cells. Annexin V-FIFC/PI test and TUNEL showed that the number of apoptotic cells of the mutant PSM146L cells was significantly higher than that off the wild type PSI cells (P < 0.05), and the number of apoptotic cells of the mutant PSM146L cells treated with ginsenoside-Rg1 was significantly lower than that of the un-treated cells (P < 0.05). Immunofluorescence staining showed that the expression site of Abeta was consistent with that of caspase-3, the protein expression levels of Abeta42 and caspase-3 of the PS1M146L/APP751 CHO cells treated with 25 micromol/L ginsenoside-Rg1 were both significantly lower than those of the untreated PS1M146L/APP751 CHO cells (P < 0.05). Western blotting showed that the active caspase-3 protein expression level of the PSIM146L cells was significantly higher than hat of the wild type PSI cells (P < 0.05) and the caspase-3 protein expression level of the PS1M146L/APP751 CHO cells treated with 25 micromol/L ginsenoside-Rg1 was significantly lower than that of the untreated PS1M146L/APP751 CHO cells (P < 0.05).


CONCLUSIONS
Ginsenoside-Rg1 prevents cells from apoptosis through inhibiting the production of Abeta42 and decreasing the expression of the active caspase-3.
Wei
Cui-Bai
CB
Department of Neurology, Xuanwu Hospital, Capital University of Medical Sciences, Beijing 100053, China.
Jia
Jian-Ping
JP
Liang
Ping
P
Guan
Yun-Qian
YQ
D016229:Amyloid beta-Peptides / Q000096:biosynthesis*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D016466:CHO Cells; D053148:Caspase 3 / Q000378:metabolism; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D006224:Cricetinae; D003412:Cricetulus; D004305:Dose-Response Relationship, Drug; D005260:Female; D036145:Ginsenosides / Q000494:pharmacology*; D009154:Mutation; D011897:Random Allocation
D016229:Amyloid beta-Peptides; D036145:Ginsenosides; D053148:Caspase 3; C035054:ginsenoside Rg1