The Inhibitory Effect Of Ginsenoside Rd On Human Gastric Cancer Cells And Its Mechanism

Objects:This study was designed to research the inhibitory effect of Ginsenoside Rd(GS-Rd)on human gastric cancer cell line SGC-7901 and MKN-45,then try to explore the pharmacological mechanism of GS-Rd on human gastric cancer.Methods:1.MTT assay was used to observe the effects of different concentrations GS-Rd on human gastric cancer cell activity in different time.2.Useing plate clone formation assay detect the influence of human gastric cells in the intervention of different concentrations GS-Rd.3.flow cytometry was used to detect the effect of different concentrations GS-Rd on human gastric cancer cell line SGC-7901 and MKN-45.4.Western blot assay was used to measure the expression of Bax、Bcl-2、Caspase-3 Caspase-9 and cyclin D1.Result:1.The proliferation of human gastric cancer cells line SGC-7901 and MKN-45 was inhibited by Ginsenoside Rd with the concentration of 40、80、120、160、200 μg/mL in dose dependent manner.also in time of 24 h,48h,72 h after found that GS-Rd with human gastric cancer cells SGC-7901 and MKN-45 has dose dependent manner,and with the increase of drug concentration and action time of extended its inhibition also obvious enhancement,and has obvious time-dose dependent,The IC50 measured at 48 h was SGC-7901 at 86.963±0.230 μg/mL and MKN-45 at 71.698±2.162 μg/mL,at 72 h the inhibitory rate of GS-Rd on the two kinds of cells reached the highest.2.The proliferation of human gastric cancer cells with Ginsenoside Rd was detected by plate cloning method.The results showed that Rd had significant inhibitory effect on the formation of two kinds of gastric cancer cell colonies.compared with control group,the cell colonies of treatment group has decreased with dose.3.Western blot assay detection expression of cyclinD1,Bcl-2 were decreased with increasing concentration of ginsenoside Rd,while the increased expression of Bax,Caspase-3,Caspase-9.Conclusion:The results showed that ginsenoside Rd had significant inhibitory effect on human gastric cancer cells SGC-7901 and MKN-45,with significant time-dose dependence.Rd also significantly promoted the apoptosis of gastric cancer cells,and its mechanism may be by up-regulating the expression of pro-apoptotic protein Bax,reducing the expression of apoptotic inhibitory protein Bcl-2,reducing the ratio of Bcl-2 /Bax,further regulating the activation of Caspase-3 in the downstream protein molecule Caspase family,activating the expression of apoptotic receptor Caspase-9,and causing apoptosis.