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机构地区:[1]西南医科大学附属医院呼吸内一科,四川泸州646000 [2]自贡市第一人民医院呼吸内科,四川自贡643000
出 处:《肿瘤基础与临床》2017年第6期468-471,共4页journal of basic and clinical oncology
摘 要:目的研究二甲双胍对人肺腺癌A549细胞的增殖抑制作用及对环氧化酶-2(COX-2)、血管内皮生长因子(VEGF)的表达影响。方法采用不同浓度(2.5、5.0、10.0、20.0、40.0 mmol·L^(-1))的二甲双胍在不同时间点(24、48、72 h)处理A549细胞,MTT检测细胞增殖,ELISA法检测细胞上清液中COX-2、VEGF的水平。结果 24 h:各实验组OD值分别为0.684±0.048、0.645±0.073、0.613±0.037、0.593±0.058、0.573±0.045,与对照组比较差异均无统计学意义(P均>0.05);48 h:各实验组OD值分别为0.681±0.057、0.613±0.032、0.557±0.065、0.506±0.063、0.453±0.034,与对照组比较差异均有统计学意义(P均<0.05);72 h:各实验组OD值分别为0.728±0.047、0.635±0.083、0.575±0.059、0.519±0.053、0.451±0.039,与对照组比较差异均有统计学意义(P均<0.05)。72 h时,实验组与对照组比较COX-2和VEGF的表达均下降,且差异均有统计学意义(P均<0.05)。结论二甲双胍能够抑制人肺腺癌A549细胞的增殖,且抑制率与二甲双胍干预的浓度和时间有关;二甲双胍能够抑制人肺腺癌A549细胞COX-2及VEGF的表达,这可能与二甲双胍抑制人肺腺癌A549细胞增殖机制有关。Objective To investigate the effect of metformin on the proliferation inhibition of human lung adenocarcinoma A549 cells and to test the expressions of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF). Methods A549 cells ware treated by metformin at different concentrations (2.5,5.0,10.0,20.0, 40.0 mmol· L-1) and at different time points (24,48,72 h). MTT assay was used to measure the cell proliferation. ELISA was used to measure the expressions of COX-2 and VEGF. Results The OD values of the experimental group were 0. 684±0.048,0.645±0. 073,0. 613±0. 037,0. 593±0. 058,0. 573±0. 045 at 24 h,there was no significant difference between all the experimental groups and the control group ( P 〉 0.05 ). The OD values of the experimental group were 0.681±0.057,0. 613±0.032,0. 557±0. 065,0. 506±0. 063,0. 453±0. 034 at 48 h, the differences between all the experimental groups and the control group were statistically significant (P 〈 0.05 ). The OD values of the experimental group were 0. 728±0. 047,0. 635 ±0. 083,0. 575±0. 059,0. 519 ± 0.053, 0.451±0.039,the differences between all the experimental groups and the control group were statistically significant ( P 〈 0.05 ). The expressions of COX-2 and VEGF in all the experimental groups were decreased at 72 h compared with the control group, and the differences were statistically significant ( P 〈 0.05 ). Conclusion Metformin can inhibithuman lung adenocarcinoma A549 cell proliferation, and the inhibition rate with time and concentration extention ; mefformin can inhibit the expressions of COX-2 and VEGF in the human lung adenocarcinoma A549 cell, which might be one of the mechanism that metformin inhibits human lung adenocarcinoma A549 cell proliferation.
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