Abstract：Objective To observe whether Survivin-siRNA can enhance the proliferation inhibition and apoptosis induction of triterpenoid extract of Prunella vulgaris L. (P. vulgaris) on esophageal cancer Eca-109 cells, and to explore its mechanism. Methods The esophageal cancer Eca-109 cells were divided into blank control group, negative control group, P. vulgaris group, siRNA transfection group, and P. vulgaris+siRNA transfection group. After 48 h of esophageal cancer Eca-109 cells in each group, the expression levels of Survivin mRNA and Survivin protein were detected by RT-PCR and Western blot. The proliferation inhibition rate of esophageal cancer cells was detected by CCK-8, and the apoptosis rate was detected by flow cytometry. Results The expression levels of Survivin mRNA and Survivin protein in esophageal cancer Eca-109 cells in the P. vulgaris group, siRNA transfection group and P. vulgaris+siRNA transfection group were lower than those in the control group and negative control group, and the differences were statistically significant (P<0.05). The esophageal cancer Eca-109 cell proliferation inhibition rate and cell apoptosis rate in the P. vulgaris group, siRNA transfection group and P. vulgaris+siRNA transfection group were higher than those in the control group and negative control group, and the differences were statistically significant (P<0.05). The expression levels of Survivin mRNA and Survivin protein in esophageal cancer Eca-109 cells in the P. vulgaris+siRNA transfection group were lower than those in the P. vulgaris group and the siRNA transfection group, and the differences were statistically significant (P<0.05). The proliferation inhibition rate and cell apoptosis rate of esophageal cancer Eca-109 cells in the P. vulgaris+siRNA transfection group were higher than those in the P. vulgaris group and siRNA transfection group, and the differences were statistically significant (P<0.05). Conclusion Survivin-siRNA can enhance the effect of Chinese herbal medicine P. vulgaris on the proliferation inhibition and apoptosis induction of esophageal cancer Eca-109 cells.
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