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作 者:杨永帆[1] 李苹苹[1] 龚媛媛[1] 胡常红[1] 周雯雯[1] 梅杰[1]
机构地区:[1]重庆医科大学附属口腔医院,重庆市口腔疾病与生物医学研究中心,重庆400001
出 处:《激光杂志》2013年第1期90-91,共2页Laser Journal
摘 要:目的:检测uPAR抗体对口腔癌HB细胞增殖的影响,并探讨其作用机制。方法:MTT法检测不同浓度的uPAR抗体(20、50、100μg/ml)作用于口腔癌HB细胞,并检测不同作用时间(24、48和72 h)的细胞增殖抑制率;流式细胞仪检测细胞周期的变化;Annexin V-FITC/PI染色法检测对细胞凋亡的影响;酶联免疫吸附法检测uPAR抗体对HB细胞分泌VEGF-D的影响。结果:uPAR抗体能抑制HB细胞的增殖,并呈现浓度和时间依赖关系。uPAR抗体可使HB细胞周期停滞于G0/G1期,随着uPAR抗体作用浓度的增加,G0/G1期细胞比例逐渐增高。uPAR抗体可促进HB细胞凋亡并呈现一定的浓度依赖关系。uPAR抗体对HB细胞分泌VEGF-D有抑制作用,随着uPAR抗体浓度的增高,其VEGF-D分泌量也逐渐降低。结论:uPAR抗体可抑制HB细胞增殖,其可能机制是使细胞周期停滞于G0/G1期,促进细胞凋亡及减少VEGF-D的分泌。Objective:To investigate the inhibitory effect of urokinase- type plasminogen activator recepior (uPAR) antibody on the proliferation of HB cells and its mechanism. Methods: HB cells were stimulated by different concentrations of uPAR antibody(20,50,100μg/ml), The cell survival rates were evaluated by MTI assay. The cell cycles were assessed by flow cytometry( FCM anlysis. Cells apoptosis was examined by flow cytometry with Annexin V - FITC/PI staining. ELISA was applied to detect the influence of uPAR antibody on the production of VEGF - D of liB cells. Results: HB cells were inhabited by ttPAR antibedy in a dose and time dependent manner, FCM analysis showed the cell cycles of HB cells were blocked at GO/G1 phase in a dose - dependent nmnner. The apoptosis assaywith Annexin V - FITC/PI showed that uPAR antibody could incluce HB cells apoptosis in a dose- dependent manner. When HB cells were treated-with differett concentrations of uPAR antibody the exudation mount of VEGF - D were lower in a dose - dependent manner. Conclusion: The proliferation of HB cells was inhibited after treatment with uPAR antibody. The inhibiting effects is caused by bloeking cell cycle pmgrsion at G0/G1 phase, inducing cells apoptosis and decreasing the exudation amount of VEGF- D.
关 键 词:uPAR抗体 口腔癌 细胞周期 细胞凋亡 VEGF-D
分 类 号:TN248.1[电子电信—物理电子学]
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