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目的：探究人参皂苷Rh2（ginsenoside Rh2，Rh2）诱导人结肠癌细胞SW480凋亡作用机制。方法 CCK-8法检测Rh2对SW480细胞增殖的影响；流式细胞术（Flow cytoMe-try，FCM）检测 Rh2对 SW480细胞凋亡的影响；Ho-echst33258染色观察Rh2对SW480细胞凋亡形态学的影响；Western blot检测经Rh2诱导 SW480细胞中凋亡相关蛋白Bcl-2、Bax、p53、cleaved caspase-3，PI3K／AKT／GSK-3β信号通路相关蛋白PI3K、AKT、P-AKT、GSK-3β、P-GSK-3β表达量变化；LY294002、Rh2单独及联合诱导 SW480细胞后，蛋白PI3K、AKT、P-AKT、GSK-3β、P-GSK-3β表达量变化。结果CCK-8结果显示 Rh2呈时间浓度依赖抑制 SW480细胞增殖。FCM结果显示细胞早期凋亡率由正常对照组的（0.70±0.09）％增至（11.06±1.04）％（P ＜0.05）。Ho-echst33258结果显示，Rh2诱导SW480细胞48h后呈现典型的凋亡形态学改变。Western blot结果显示，经Rh2诱导的SW480细胞，凋亡相关蛋白 Bcl-2表达降低，Bax、p53、激活型胱天蛋白酶3（cleaved caspase-3）蛋白表达增加；PI3K／AKT／GSK-3β信号通路蛋白PI3K、P-AKT、P-GSK-3β表达量与对照组比较明显减少，AKT、GSK-3β表达量无明显变化；LY294002、Rh2和 LY294002与 Rh2联合诱导 SW480细胞后，总 AKT 蛋白和总 GSK-3β蛋白表达量基本一致， LY294002与Rh2联合用药对SW480细胞中PI3K、P-AKT和P-GS K-3β的表达抑制作用较单独用药更加明显。结论Rh2可能是通过抑制PI3K／AKT／GSK-3β通路，激活p53信号通路，激活caspase-3，破坏Bcl-2／Bax比例，诱导结肠癌细胞SW480凋亡。“,”Aim To investigate the effect of Ginsen-oside Rh2 on apoptosis in human colorectal cancer cell SW480,and to explore the possible mechanism of it. Methods The proliferation activity of SW480 treated with Ginsenoside Rh2 was measured CCK-8 assay.Ap-optosis rates were evaluated by FCM.Hoechst 33258 staining was used to observe cell nucleus morphologi-cal;change SW480 cells were treated with Ginsenoside Rh2,and the protein expressions of Bcl-2,Bax,p53, cleaved caspase-3 ,PI3 K,AKT,P-AKT,GSK-3β,P-GSK-3βwere detected by Western blot;SW480 cells were treated with LY294002,Rh2,LY294002+Rh2, the expressions of PI3 K,AKT,P-AKT,GSK-3β,P-GSK-3βwere detected by Western blot.Results The proliferation of SW480 cells was significantly inhibited by Ginsenoside Rh2 in dose-dependent and time-de-pendent manner.FCM showed the inducing apoptosis effect of Ginsenoside Rh2 was significantly different from that of control group.Hoechst 33258 staining in-dicated clearly cell apoptosis in Ginsenoside Rh2 treat-ment groups.Western blot showed Ginsenoside Rh2 decreased expression of Bcl-2,increased expression of Bax,p53 and cleaved caspase-3,PI3K/AKT/GSK-3βpathway proteins PI3 K,P-AKT,P-GSK-3βdecreased obviously,AKT and GSK-3βwere not changed signifi-cantly in SW480.SW480 cells were separately treated with LY294002,Rh2,LY294002 +Rh2,there were no significant difference in AKT and GSK-3βprotein a-mong all groups,and the expression of PI3 K,P-AKT, P-GSK-3βdecreased more obviously in LY294002 +Rh2 group compared with LY294002 and Rh2 alone. Conclusion Rh2 induces colorectal cancer cell apop-tosis through PI3 K/AKT/GSK-3βpathway,which ac-tivates p53 and cleaved caspase-3,and destroys the balance of Bcl-2/Bax.