Abstract: Objective To study the effect of ginsenoside Rg1 on intestinal IEC-6 cells injury induced by radiation and the mechanism of PI3K/AKT pathway. Methods IEC-6 cells of rats were subcultured and divided into blank group,model group,Rg1 group and Rg1+LY294002 group.Except the blank group,rats in other groups were irradiated with ⁶⁰Co-gamma rays at a dose of 4 Gy.CCK8 method was used to detect the cell proliferation activity at 12 h,24 h and 36 h after irradiation.The survival and apoptosis status of IEC-6 cells were measured by flow cytometry.Western blot （WB） was used to detect the expression of phosphorylated AKT （p-AKT）,B-cell lymphoma-2 （Bcl-2） and Bcl-2 associated X Protein （Bax）,and the difference in Bax/Bcl-2 was compared between different groups. Results CCK-8 assay results showed that the viability of model group and Rg1+LY294002 group was lower than that of blank group and Rg1 group at 12 h and 24 h after irradiation （P<0.05）,but no significant difference was detected between the former two or the latter two groups （P>0.05）.Apoptotic test results showed that the cell viability decreased and apoptotic rate increased in all irradiation groups after irradiation,and the cell viability of model group and Rg1+LY294002 group was significantly lower than that of blank group and Rg1 group at 12 h and 24 h （P<0.05）,while the apoptotic rate at 12 h was higher than that in blank group and and Rg1 group （P<0.05）.At 36 h,the survival rate and apoptotic rate of model group and Rg1 group were similar to those of blank group （P>0.05）;compared with the former 3 groups,the Rg1+LY294002 group had similar survival rate at 36 h,but significantly higher apoptotic rate （P<0.05）.WB assay showed that p-AKT and Bcl-2 in model group and Rg1+LY294002 group were significantly lower than that in blank group and Rg1 group （P<0.05）;the ratio of Bax and Bax/Bcl-2 in model group and Rg1+LY294002 group was higher than that in blank group and Rg1 group （P<0.05）. Conclusion Ginsenoside Rg1 can effectively promote the survival and inhibit apoptosis of intestinal IEC-6 cells induced by radiation,and its mechanism may be related to the promotion of PI3K/AKT related factors.