和胃降逆胶囊对胃腺癌细胞凋亡的影响及其机制OACSTPCD

Objective To observe the effects of serum containing Hewei Jiangni on proliferation and apoptosis of gastric cancer cells(AGS)and its mechanism based on NF-κB/EMT signaling pathway.Methods Serums containing low,medium,and high concen-trations of Hewei Jiangni(3,6,and 12 g/kg)were prepared,and the blank serum was used as control group.AGS cells were intervened with serums containing different concentrations of Hewei Jiangni for 24,48,72 h respectively.The proliferation of AGS cells was detected by CCK-8 kit.The apoptosis of AGS cells was detected by DAPI staining.The migration of AGS cells was observed by Scratch test.The mRNA levels of NF-κB and EMT marker proteins E-cadherin and Vimentin were detected by quantitative real-time polymerase chain reaction(RT-qPCR).The protein expressions of NF-κB,E-cadherin,and Vimentin were detected by Western blot.Results At the same time points,compared with control group,the viability of cells was dose-dependently decreased in Hewei Jiangni groups(P＜0.01).Compared with 24 h,the viability of AGS cells was decreased in Hewei Jiangni groups at 48,72 h(P＜0.05).At 48 h,compared with control group,the apoptosis of AGS cells was dose-dependently increased in Hewei Jiangni groups(P＜0.05).Compared with control group,the scratch healing speed was slowed down,and the rate of cell migration was reduced in Hewei Jiangni groups(P＜0.05).Compared with control group,the migration was decreased at 24 h in high dose group(P＜0.01),and was also reduced at 48 h in medium and high dose groups(P＜0.01).Compared with control group,the mRNA levels of NF-κB and Vimentin in AGS cells were dose-dependently downregulated in Hewei Jiangni groups(P＜0.05),while E-cadherin mRNA was dose-dependently upregulated(P＜0.01).Compared with control group,the protein levels of NF-κB and Vimentin in AGS cells were dose-dependently downregulated while the E-cadherin proein expression was dose-dependently upregulated in Hewei Jiangni groups(P＜0.05).Conclusion Hewei Jiangni can mediate the migration and invasion of AGS cells by inhibiting the activation of NF-κB,and regulating the expressions of downstream EMT-related proteins,thus inhibiting the proliferation and promoting the apoptosis of AGS cells.