Abstract: Objective To study the effects of Radix Actinidiae extractives on the proliferation and apoptosis of esophagus cancer cell line EC109 and to explore its mechanism.Methods EC109 cells were cultured in vitro.The cells were treated with different doses of Radix Actinidiae extractives.3-4,5-dimethylthylthiazol-2-yl-2,5 diphenyltetrazolium bromide (MTT) assay was used to detect the inhibition of the cells.Cell apoptosis was measured by flow cytometry(FCM).Immunohistochemistry(S-P) was used to detect the expression of Bcl-2,Bax protein of EC109 cell after the treatments.Intercellular calcium level was measured with laser scanning confocal microscopy.Results Radix Actinidiae extractives had obviously inhibitive effect on EC109 cell in a dose-and time-dependent manner in vitro.Inhibition rate(IR) (from 5.2% to 56.77%) and apoptosis index(AI) (from 7.05% to 51.11%) increased in a dose-and time-dependent manner with significant differences compared to those of the control group(P< 0.05).The expression of Bcl-2 protein of EC109 cell was decreased in a dose-and time-dependent manner.The expression of Bax protein of EC109 cell increased progressively also in a dose-and time-dependent manner.There was no change in the control group.Significant differences were observed in the groups of the different dose(≥100 μg/mL) and different treatment time(≥48 hr) compared to the control group(P< 0.05 for all).Intercellular calcium level of the control group was constant,but obviously increased in the treatment groups in a dose-dependent manner with a peak at 12 hr(P< 0.05).Conclusion Radix Actinidiae extractives has evident inhibition effect on esophagus cancer cell line EC109 in a dose-and time-dependent manner in vitro.It could also induce the apoptosis of EC109 cell in a dose-and time-dependent manner in vitro.Radix Actinidiae extractives could dow n-regulate the expression of Bcl-2 and up-regulate the expression of Bax protein level.The increased intercellular calcium promotes apoptosis.The mechanism of the induced apoptosis may be mediated by the regulation of the expression of apoptosis regulation gene and the level of intercellular calcium.