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机构地区:[1]遵义医学院附属口腔医院口腔外科,贵州遵义563000 [2]遵义医学院,贵州遵义563000
出 处:《贵州医药》2013年第2期121-123,共3页Guizhou Medical Journal
基 金:贵州省卫生厅资助项目(D-291);贵州省遵义市红花岗区科技局资助项目(E-052)
摘 要:目的探讨熊果酸对口腔鳞状细胞癌(Tca8113)的生长抑制情况及其对细胞周期和凋亡的作用。方法用浓度0、10、20、30、40、50μmol/L的熊果酸对口腔鳞状细胞癌进行干预,MTT法检测细胞增殖活性,流式细胞仪分析细胞周期,Annexin-V-FITC/PI双染流式细胞仪定量检测细胞凋亡。结果 (1)熊果酸对Tca8113细胞的增殖抑制具有时间--剂量依赖性,各实验组细胞增殖抑制率与对照组比较差异具有统计学意义(P<0.05)。(2)各浓度组熊果酸将细胞阻滞于S期,浓度30、40、50μmol/L的熊果酸总凋亡率分别为30.76%、43.77%及70.15%,与对照组比较差异有统计学意义(P<0.05)。结论熊果酸在体外抑制口腔鳞状细胞癌生长,呈时间--剂量依赖性,并阻滞细胞周期,促进细胞凋亡。Objective To investigate the effects of Ursolic acid on the proliferation of oral squa- mous cell carcinoma (TcaSll3) and cell cycles and apoptosis. Methods Oral squamous cell carcinoma was intervened with 0,10,20,30,40 and 50μmol/L UA. The cell proliferation activity was measured by MTT assay, cell cycles were analyzed by flow cytometry, and the cell apoptotic rates were detected by flow cytometry through Annexin-V-FITC/PI staining. Results A time- and dose-dependent inhibition were detected in TcaS113 cells that were treated with different concentrations of UA for 24, 72 and 120 h, and there were statistically significant differences of proliferative inhibition between the control and the treated groups (P 〈 0. 05). Cell cycles arrest in S, and cell apoptosis rate was 30.76 %,43.77% and 70.15% UA treatment for 24,72 and I20 h, and there were statistically signifi- cant differences(P〈 0. 05). Conclusion UA inhibits the growths of oral squamous cell carcinoma, time- and dose-dependent, and block cell cycles and promotes cell apoptosis.
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