Rg1 protects rat bone marrow stem cells against hydrogen peroxide-induced cell apoptosis through the PI3K/Akt pathway.

Abstract

The aim of the present study was to investigate the protective mechanism of ginsenoside Rg1 against the apoptosis of rat bone marrow stem cells (rBMSCs) under oxidative stress, and to determine the association with the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) pathway. H2O2 was used to induce oxidative injury in rBMSCs. The cells in the H2O2 model group were treated with 800 µM H2O2 for 6 h to induce oxidative injury. The cells in the ginsenoside Rg1 group were treated with 10 µM ginsenoside Rg1 for 24 h, followed by H2O2 treatment. The cells in the Akt pathway blockage group were treated with 25 µM LY294002 for 1 h, followed by ginsenoside Rg1 + H2O2 treatment. The cell counting kit-8 assay was performed to determine cell viability. Cell apoptosis was detected by flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. The results of flow cytometry and TUNEL staining indicated that the apoptotic rate of the H2O2 model group was significantly higher compared with that of the control group. Following the ginsenoside Rg1 pretreatment, the apoptotic rate was significantly reduced. In the Akt pathway blockage group, no significant alterations in the levels of cell apoptosis were observed compared with the H2O2 model group. Western blot analysis demonstrated that the ginsenoside Rg1 group had a significant downregulation of Bax and cleaved caspase‑3 and an upregulation of Bcl‑2 and phosphorylated Akt protein expression levels compared with the H2O2 model group and the Akt pathway blockage group. In conclusion, ginsenoside Rg1 had a protective effect against the H2O2‑induced oxidative stress of rBMSCs, and the specific mechanism may be associated with the activation of the PI3K/Akt pathway by ginsenoside Rg1.