The Antagonism Of Atractylenolide Ⅰ On Paclitaxel Increasing Survivin Expression And Promoting Apoptosis In Ovarian Cancer Cell

Objective:To study the antagonism of atractylenolide I on paclitaxel increasing survivin expression and promoting apoptosis in ovarian cancer cell.Methods:Reverse Transcription Polymerase Chain Reaction(RT-PCR) was used to detect the transcription levels of survivin mRNA and Flow CytoMeter Annexin V-FITC/PI was used to deterninate early apoptosis of tumer cells that were human ovarian cancer SKOV-3 cell lines(TLR-4/MyD88+) and A2780 cells lines (TLR-4/MyD88-) which were induced by different concentrations of LPS, paclitaxel, atractylenolide I alone and jion with paclitaxel for 24 hours.Results:RT-PCR:①Both of SKOV-3 cell lines(TLR-4/MyD88+) and A2780 cells lines(TLR-4/MyD88-) could transcript survivin mRNA.②LPS induced a significant dose-dependent increase of survivin mRNA in SKOV-3 cells, about 0.3～1 times than controls (p<0.05). But A2780 cells did not change significantly (p>0.05).③Paclitaxel induced a significant dose-dependent increase of survivin mRNA in SKOV-3 cells, about 0.16-0.7 times than controls (p<0.05). But A2780 cells did not change significantly (p>0.05).④There were not significantly change of survivin mRNAs both in SKOV-3 cells and A2780 cells which were induced by atractylenolide I alone (p>0.05).⑤Atractylenolide I jion with paclitaxel induced a significant dose-dependent decrease of survivin mRNA in SKOV-3 cells, about 0.13-0.39 times than paclitaxel alone(p<0.05). But A2780 cells did not change significantly (p>0.05). Flow CytoMeter:different concentrations of atractylenolide I jion with paclitaxel induced a significant dose-dependent decrease of early apoptosis in SKOV-3 cells than paclitaxel alone,(9.9±0.82,11.6±1.76; p=0.002,0.001). But A2780 cells did not change significantly (p=0.336,0.593)Conclusion:There is a paclitaxel—TLR-4/MyD88+—survivin pathway in the MyD88+human ovarian cancer cells which regulate the apoptosis of tumor cells. This pathway could be activated by LPS or paclitaxel and could inhibite tumor cell apoptosis to a certain extent. By antagonizing the paclitaxel—TLR-4/MyD88+— survivin pathway atractylenolide I could derease the express of survivin and promoting tumor cells apoptosis. The above phenomenon did not appear in A2780 cells which were MyD88-.