Nitidine chloride induced in vitro human oral squamous cell carcinoma KB cells in G2 - M phase arrest and apoptosis of.docVIP

 PAGE \* MERGEFORMAT 4 Nitidine chloride induced in vitro human oral squamous cell carcinoma KB cells in G2 / M phase arrest and apoptosis of Author: Liu Gang Wang Bo Long Hai Yang Qin 3 [Abstract] Objective To investigate the nitidine chloride on human oral squamous cell carcinoma KB cell cycle and apoptosis and their interaction. Methods MTT colorimetric assay nitidine chloride inhibition of cell proliferation; flow cytometry (FCM) detection nitidine chloride on cell cycle; Hoechst33258 detect cell apoptosis; transmission electron microscope observation of cells, Advanced Micro DevicesFrame . Results nitidine chloride concentration-dependent manner in vitro was significantly inhibited KB cell growth, 48 h IC50 of (2.36 ± 0.22) μ g / ml; compared with the control group, after 3μ g/ml nitidine chloride effect, G2 / M phase cell ratio significantly increased; 6 μ g / ml, when the highest proportion of apoptotic cells, showing a typical nuclear chromatin condensation, fragmentation; 9 μ g / ml, the apoptosis rate decreased, while microscope, a large number of necrotic cells . Conclusion nitidine chloride against KB cells in a way closely related to its dose, low concentrations in G2 / M phase arrest mainly in the concentration-induced apoptosis is caused by its high concentration of necrosis. [Keywords:] nitidine chloride G2 / M phase arrest apoptosis in KB cells, necrotic Abstract: ObjectiveTo explore the influence of nitidine chloride on cell cycle and apoptosis of human carcinoma of mouth floor KB cells and their relationship.MethodsThe proliferation inhibition rate and IC50 (48 h) of nitidine chloride to KB cells were examined by MTT assay. The influence of nitidine chloride on cell cycle was measured by flow cytometry. Hoechst33258 technology was adopted to detect cell apoptosis. Transmission electron microscope was used to observe cell ultrastructure.ResultsNitidine chloride markedly suppressed proliferation of KB cells in a dose-dependent manner in