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作 者:常悦[1] 王维嘉[2] 朴军颜[3] 姚珂[3] 左非非 徐少博[3] 徐霞[3]
机构地区:[1]郑州大学口腔医学院正畸科,郑州450052 [2]郑州大学临床医学系,郑州450001 [3]郑州大学药学院,郑州450001
出 处:《郑州大学学报(医学版)》2015年第3期413-416,共4页Journal of Zhengzhou University(Medical Sciences)
摘 要:目的:观察冬凌草提取物KYBNZ-1I对口腔鳞状细胞癌细胞Tca8113增殖的抑制作用,并探讨其可能机制。方法:采用MTT法检测0.5、1.0、2.0、4.0、8.0 mg/L的KYBNZ-1I分别作用24、48、72 h对Tca8113细胞增殖的抑制作用。分别采用流式细胞仪及Western blot检测0.0、1.0、2.0、3.0 mg/L的KYBNZ-1I作用48 h Tca8113细胞的周期分布、凋亡情况及CyclinD 1、CyclinB 1、Cdc-2蛋白的表达。结果:KYBNZ-1I对Tca8113细胞增殖有抑制作用,该作用呈剂量和时间依赖性(F剂量=133.991,F时间=22.526,P<0.05)。与对照组比较,1.0、2.0、3.0 mg/L的KYBNZ-1I作用48 h后G2/M期细胞增多,并可诱导细胞凋亡,呈剂量依赖性(F=108.465、212.353,P<0.05);随药物剂量的升高,CyclinD 1蛋白的表达水平下降(F=45.288,P<0.001),CyclinB 1、Cdc-2蛋白的表达水平升高(F=21.273、19.228,P<0.05)。结论:KYBNZ-1I对Tca8113细胞增殖有抑制作用,可将细胞阻滞于G2/M期并诱导细胞凋亡,其作用机制可能与KYBNZ-1I抑制CyclinD 1蛋白的表达、提高CyclinB 1和Cdc-2蛋白的表达有关。Aim: To investigate the effect of KYBNZ-1I on proliferation of oral squamous cell carcinoma cell line Tca8113 and the possible mechanism. Methods: The effect of KYBNZ-1I( 0. 5,1. 0,2. 0,4. 0 and 8. 0 mg / L) on proliferation of Tca8113 cells for 24,48 and 72 h was measured by MTT assay. Tca8113 cells were treated by 0. 0,1. 0,2. 0 and 3. 0 mg /L KYBNZ-1I for 48 h,then flow cytometry and Western blot were used to detect the cell cycle distribution,apoptosis and the expressions of Cyclin D1,Cyclin B1 and Cdc-2. Results: KYBNZ-1I inhibited the proliferation of Tca8113 cells in a time and dose dependent manner( Fdose= 133. 991,Ftime= 22. 526, P〈0. 05). Compared with control group,the percentage of G2/ M phase Tca8113 cells was significantly higher( F = 108. 465, P〈0. 001),and cell apoptosis rate raised( F = 212. 353, P〈0. 001) in a dose-dependent manner. With the increase of KYBNZ-1I concentration,the expression of Cyclin D1 decreased( F =45. 288, P〈0. 001),and the expressions of Cyclin B1 and Cdc-2 increased( F =21. 273 and 19. 228, P〈0. 05). Conclusion: KYBNZ-1I could inhibit proliferation,arrest the cells at G2/ M phase and induce cell apoptosis,which may be explained by its restraining expression of Cyclin D1,and upregulating expressions of Cyclin B1 and Cdc-2.
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