论文部分内容阅读
目的 探讨TNP 4 70对肺腺癌细胞增殖和凋亡的影响及其作用机制。方法 以不同浓度的TNP 4 70作用于培养的肺腺癌AGZY 82A细胞株 ,以免疫组化S P法检测肺腺癌细胞增殖细胞核抗原 (PCNA)、p5 3、bcl 2、血管内皮生长因子 (VEGF)和VEGF受体Flk 1的表达。结果 随着TNP 4 70浓度的增加 ,肺腺癌细胞VEGF、Flk 1、PCNA的表达减少 ,p5 3、bcl 2的表达逐渐增加 ;当TNP 4 70为 10 7μg/L时 ,细胞增殖几乎停止。随着TNP 4 70 (10 4μg/L)作用时间的延长 ,肺腺癌细胞VEGF、Flk 1、PCNA的表达逐渐减少 ,而p5 3、bcl 2的表达逐渐增加。结论 TNP 4 70通过使肺腺癌细胞自分泌VEGF减少 ,Flk表达降低 ,从而抑制肺腺癌细胞增殖 ,促进其凋亡。
Objective To investigate the effect of TNP 4 70 on proliferation and apoptosis of lung adenocarcinoma cells and its mechanism. Methods AGZY 82A cells were cultured with different concentrations of TNP 4 70. The expression of proliferating cell nuclear antigen (PCNA), p5 3, bcl 2 and vascular endothelial growth factor (VEGF) in lung adenocarcinoma cells were detected by immunohistochemical SP method. ) And VEGF receptor Flk 1 expression. Results With the increase of TNP 4 70 concentration, the expression of VEGF, Flk 1 and PCNA in lung adenocarcinoma cells decreased and the expressions of p5 3 and bcl 2 increased gradually. When TNP 4 70 was 10 7 μg / L, cell proliferation almost stopped. The expression of VEGF, Flk 1 and PCNA in lung adenocarcinoma cells decreased gradually with the prolongation of TNP 4 70 (10 4 μg / L), while the expression of p5 3 and bcl 2 gradually increased. CONCLUSION: TNP 4 70 can inhibit the proliferation and promote the apoptosis of lung adenocarcinoma cells by decreasing the autocrine VEGF and decreasing the expression of Flk.