论文部分内容阅读
AIM:To illustrate the possible role of cell differential agent-Ⅱ(CDA-Ⅱ)in the apoptosis of hepatoma cells induced byarsenic trioxide(As_2O_3).METHODS:Hepatoma cell lines BEL-7402 and HepG2 weretreated with As_2O_3 together with CDA-Ⅱ.Cell survivingfraction was determined by MTT assay;morphologicalchanges were observed by immunofluorescence staining ofHoechst 33 258;and cell cycle and the apoptosis index weredetermined by flow cytometry(FCM).RESULTS:Cytotoxity of CDA-Ⅱ was low.Nevertheless,CDA-Ⅱ could strongly potentiate arsenic trioxide-inducedapoptosis.At 1.0 g/L CDA-Ⅱ,IC_(50)of As_2O_3 in hepatoma celllines was reduced from 5.0μmol/L to 1.0μmol/L(P<0.01).The potentiation of apoptosis was dependent on the dosageof CDA-Ⅱ.FCM indicated that in hepatoma,cell growth wasinhibited by CDA-Ⅱ at lower concentrations(<2.0 g/L)primarily by arresting at S and G_2 phase,and at higherconcentrations(>2.0 g/L)apoptotic cell and cell cyclearresting at G_1 phase increased proportionally.Thecombination of two drugs led to much higher apoptotic rates,as compared with the either drug used alone.CONCLUSION:CDA-Ⅱ can strongly potentiate As_2O_3-induced apoptosis in hepatoma cells,and two drugs canproduce a significant synergic effect.
AIM: To illustrate the possible role of cell differential agent-Ⅱ (CDA-Ⅱ) in the apoptosis of hepatoma cells induced byarsenic trioxide (As_2O_3) .METHODS: Hepatoma cell lines BEL-7402 and HepG2 weretreated with As_2O_3 together with CDA-Ⅱ. Cell surviving fraction was determined by MTT assay; morphological changes were observed by immunofluorescence staining of Hoechst 33 258; and cell cycle and the apoptosis index were determined by flow cytometry (FCM) .RESULTS: Cytotoxity of CDA-II was low. potentiate of arsenic trioxide- induced apoptosis. At 1.0 g / L CDA-II, IC 50 (50) of As 2 O 3 in hepatoma celllines was reduced from 5.0 μmol / L to 1.0 μmol / dosageof CDA-II.FCM indicated that in hepatoma, cell growth was inhibited by CDA-II at lower concentrations (<2.0 g / L) arrest by at arresting at S and G_2 phase, and at higher concentrations (> 2.0 g / L) cell cyclearresting at G_1 phase increased proportional ly.Thecombination of two drugs led to much higher apoptotic rates, as compared with the either drug used alone. CONCLUSION: CDA-II can strongly potentiate As_2O_3-induced apoptosis in hepatoma cells, and two drugs canproduce a significant synergic effect.