人参皂苷Rg3通过PI3K/Akt信号通路抑制胶质母细胞瘤的增殖和迁移OA

Objective To investigate the mechanism by which ginsenoside Rg3 inhibits malignant biological behaviors of glioblastoma through regulating the phosphatidylinositol 3-kinase/protein kinase B(PI3K/Akt)signaling pathway.Methods U87MG cells were randomly divided into a control group,low-dose group(25 μmol/L Rg3),and high-dose group(50 μmol/L Rg3).After 12 h and 24 h of intervention,CCK-8 assay and Transwell migration assay were employed to evaluate cell proliferation and invasion/migration capabilities.The mRNA and protein expression levels of PI3K and Akt were quantified using qRT-PCR and immunofluorescence.Results Ginsenoside Rg3 significantly suppressed U87MG cell proliferation and migration.compared with the control group,migrated cell numbers markedly decreased at 12 h in both dose groups(P<0.01).Upon extending intervention to 24 h,both cell viability and migration counts in treatment groups exhibited significant reductions compared to the control and 12 h groups(P<0.01),with the high-dose group demonstrating stronger inhibition than the low-dose group at the same timepoint(P<0.01).Mechanistic studies revealed that ginsenoside Rg3 downregulated key PI3K/Akt pathway molecules in a time-and dose-dependent manner.At 12 h,the high-dose group showed significantly reduced PI3K and Akt mRNA expression(P<0.01),accompanied by decreased immunofluorescence intensity of both proteins in both dose groups(P<0.01).By 24 h,the inhibitory effects became more pronounced(P<0.01),with superior suppression observed in the high-dose group compared to its low-dose counterpart(P<0.05).Conclusion Ginsenoside Rg3 inhibits glioblastoma proliferation and migration via the PI3K/Akt signaling pathway,demonstrating time-and concentration-dependent effects.