人参皂苷Rg1对MDA诱导小鼠间充质干细胞凋亡的保护作用

目的：观察人参皂苷Rg1 （Ginsenoside Rg1,GS-Rg1）对丙二醛（Malondialdehyde,MDA）诱导的小鼠骨髓间充质干细胞（Mesenchymal stem cells,MSCs）凋亡的保护作用,并探讨其作用的可能机制.方法：以不同剂量（10、50、100 mg/L）人参皂苷Rg1预处理24 h,在小鼠骨髓MSC体外培养体系中加入MDA,TUNEL法,流式细胞术检测MSC凋亡率,Q-RT-PCR和Westen印迹分析检测Bcl-2、Bax和Caspase-3表达.结果：GS-Rg1可以减少TUNEL阳性细胞百分率及亚G1峰凋亡细胞百分率,增加Bcl-2mRNA及蛋白的表达水平,降低Bax和Caspase-3mRNA及蛋白表达水平.结论：GS-Rg1对MDA诱导小鼠间充质干细胞凋亡具有保护作用,其作用机制可能与增加Bc1-2表达,降低Bax和Caspase-3表达有关.

Protective Effect of Ginsenoside Rg1 on MDA-induced Apoptosis in Mesenchymal Stem Cells Derived from Murine Bone Marrow

Aim the present study was designed to investigate the cytoprotective effects of ginsenoside Rgl against ma- londialdehyde（MDA） induced apoptosis in the mesenchymal stem cells （MSC） and its possible mechanisms in vitro. Methods Murine bone marrow-derived mesenchymal stem cells were incubated with MDA after being treated with GS-Rgl （10, 50, 100 mg/L） for 24 h in vitro, the apoptotic rate detected by a flow cytometry analysis and TUNEL assay, the expression of Bcl-2, Bax and Caspase-3 of MSC were examined by Q-RT-PCR and Westen blotting. Results The percent- age of TUNEL-positive cells and percentage of cells of a sub-G1 peak decreased significantly in MSC pretreated with GS- Rgl. GS-Rgl pre-treatment decreased the expression of pro-apoptotic gene Bax and Caspase-3, whereas it increased the expression of anti-apoptotic gene Bcl-2. Conclusion GS-Rgl protect MSCs from MDA-induced apoptosis. The protective mechanism could be related to its ability to increase the expression of Bcl-2, reduce the expression of Bax, and inhibite the expression ~f Caspase-3.