| 马春兰,张宝亮,刘晓明.雷公藤多苷抑制 PI3K/AKT信号通路对肺腺癌细胞迁移和血管形成的影响[J].安徽医药,2022,26(2):235-238. |
| 雷公藤多苷抑制 PI3K/AKT信号通路对肺腺癌细胞迁移和血管形成的影响 |
| Effects of tripterygium glycosides on migration and angiogenesis of lung adenocarcinoma cell by inhibiting PI3K/AKT signaling |
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| DOI：10.3969/j.issn.1009-6469.2022.02.006 |
| 中文关键词: 腺癌，细支气管肺泡 雷公藤多苷 磷脂酰肌醇 3-激酶 蛋白激酶 B 迁移 血管生成 |
| 英文关键词: Adenocarcinoma,bronchiolo-alveolar Tripterygium wilfordii polyglycosidium Phosphatidylinositol 3-kinase Protein kinase B Migration Angiogenesis |
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| 中文摘要: |
| 目的探讨雷公藤多苷( TWP)对肺腺癌 A549细胞迁移、血管生成及磷脂酰肌醇 3-激酶 /蛋白激酶 B(PI3K/AKT)信号通路的影响。方法人肺腺癌细胞株 A549体外培养，分别用 TWP(0、20、40、80 μmol/L)处理 24、48和 72 h，采用 CCK-8法、流式细胞仪和 Transwell法分别检测 A549细胞的增殖、凋亡和迁移情况， Matrigel胶小管形成实验检测血管生成情况，蛋白质印迹法(Western blotting)检测 A549细胞中 PI3K、磷酸化 PI3K(p-PI3K)、 AKT、磷酸化 AKT(p-AKT)蛋白表达情况。结果随培养时间延长， 20、40、80 μmol/L TWP组 A549细胞增殖抑制率均显著升高( P<0.05)； 20、40、80 μmol/L TWP组 A549细胞凋亡率［( 8.78±0.69)%、(10.36±1.13)%、(21.68±2.11)%］均显著升高( P<0.05)，穿膜细胞数［( 122.08±30.72)、(83.34±19.75)、(43.58± |
| 英文摘要: |
| Objective To investigate the effects of tripterygium wilfordii polyglycosidium (TWP) on migration, angiogenesis and phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway of lung adenocarcinoma A549 cells.Methods Human lung adenocarcinoma cell line A549 was cultured in vitro and treated with TWP (0, 20, 40, 80 μmol/L) for 24, 48 and 72 hours, respec.tively, the proliferation of A549 cells was detected by CCK-8 method, the apoptosis of A549 cells was detected by flow cytometry, themigration of A549 cells was detected by Transwell method, the angiogenesis was detected by the Matrigel tubule formation experiment,and the expressions of PI3K, p-PI3K, AKT and p-AKT in A549 cells were detected by Western blot.Results The proliferation inhibi.tion rate of A549 cells in 20, 40 and 80 μmol/L TWP groups increased significantly with the increase of culture time (P<0.05); theapoptosis rate of A549 cells in 20, 40 and 80 μmol/L TWP groups increased significantly [(8.78±0.69) %,(10.36±1.13) %, (21.68±2.11) % , P<0.05], while the number of transmembrane cells [(122.08±30.72), (83.34±19.75), (43.58±13.29)], p-PI3K/PI3K ratio [ (0.76±0.13),(0.55±0.12), (0.36±0.09)] and p-AKT/AKT ratio [(0.53±0.14), (0.35±0.09),(0.21±0.05)] decreased significantly (P<0.05);the number of tubes of human umbilical vein endothelial cells (HUVECs) induced by A549 cells in 0, 20, 40 and 80 μmol/L TWPgroups was significantly higher than that in the control group [(35.85±8.72), (24.13±6.86), (15.34±4.66), (9.15±2.25) vs. (6.31±1.49), P< 0.05], while the number of HUVEC tubes induced by A549 cells decreased significantly with the increase of TWP concentration (P< 0.05).Conclusion TWP may inhibit the proliferation, migration, angiogenesis and apoptosis of lung adenocarcinoma A549 cells by in.hibiting the activation of PI3K/AKT signaling pathway. |
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