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作 者:洪正东[1] 史子敏[1] 朱安义[1] 林双泉[1] 刘利珍[2]
机构地区:[1]南昌大学第二附属医院泌尿外科江西省重点分子医学实验室,南昌330006 [2]南昌大学第二附属医院肿瘤内科
出 处:《临床泌尿外科杂志》2009年第1期60-63,共4页Journal of Clinical Urology
摘 要:目的:研究人参皂苷Rg3对人前列腺癌细胞株PC-3中EphB4及抗凋亡蛋白bcl-xl表达的影响。方法:用浓度为0、5、10、20和40μmol/L的人参皂苷Rg3处理PC-3细胞24 h,然后采用四甲基偶氮唑盐(MTT)方法检测人参皂苷Rg3对PC-3细胞增殖的抑制作用,用倒置显微镜和流式细胞术观察人参皂苷Rg3对PC-3细胞凋亡的诱导作用,用RT-PCR和Western blot方法检测经不同浓度人参皂苷Rg3处理后PC-3细胞中EphB4和bcl-xl的表达情况。结果:5、10、20和40μmol/L的人参皂苷Rg3对PC-3细胞增殖的抑制率分别为20.93%、31.32%、51.63%、65.43%。5~40μmol/L的人参皂苷Rg3处理细胞呈明显的凋亡形态学改变,40μmol/L人参皂苷Rg3处理PC-3细胞24 h后,凋亡细胞占(12.10±1.2)%,处理组比正常对照组(3.18±2.1)%凋亡明显增加,差异有统计学意义(P<0.05)。结论:不同浓度人参皂苷Rg3处理PC-3细胞24后,EphB4的表达随人参皂苷Rg3浓度的增加而逐渐减弱,而且bcl-xl的表达随人参皂苷Rg3浓度的增加逐渐减弱。Objective:To investigate the effects of Ginsenoside Rg3 on the expression of EphtM and antiapoptotic proteins: bcl-xl in human prostate cancer cell line PC-3. Methods: PC-3 cells were exposed to 0,5,10,20 and 40 μmol/L Ginsenoside Rg3 for 24 hours. The effect of Ginsenoside Rg3 on cell proliferation was measured by methyl thiazolyl tetrazolium (MTT) assay. The induction of Ginsenoside Rg3 for the apoptosis of PC-3 cells was observed by invert microscope and flow cytometry. The expression of EphB4 and bcl-xl were measured by RT- PCR and Western blot. Results:The inhibitory rate was 20.93% ,31.32% ,51.63% ,65.43% respectively, as PC- 3 cells were exposed to 5,10, 20 and 40 μmol/L Ginsenoside Rg3 for 24 hours. Typical morphological changes of apoptosis were induced by Ginsenoside Rg3 at the concentratations(5-40μmol/L) and flow cytometry showed the apoptosis rate was (3.18 ± 2.1)% in the normal control cells and (12.10 ± 1.2)% in the cells exposed to 40 μmol/ L Ginsenoside Rg3 for 24 hours. The apoptosis rate in the cells exposed to 40 μmol/L Ginsenoside Rg3 for 24 hours was obviously higher than the control group, (P〈0.05). Conclusions: After PC-3 cells were exposed by different concentrations ginsenoside Rg3, the expression of EphB4 and the expression of bcl-xl, decreased with the increase in the concentration of ginsenoside Rg3.
关 键 词:前列腺癌 人参皂苷RG3 受体酪氨酸激酶EphB4 凋亡
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