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、80μmol/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(Westernblotting)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、80μmol/LTWP组A549细胞增殖抑制率均显著升高(P<0.05);20、40、80μmol/LTWP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±13.29)个]、p-PI3K/PI3K比值[(0.76±0.13)、(0.55±0.12)、(0.36±0.09)]、p-AKT/AKT比值[(0.53±0.14)、(0.35±0.09)、(0.21±0.05)]均显著降低(P<0.05);0、20、40、80μmol/LTWP组A549细胞诱导静脉内皮细胞(HUVEC)成管数量较对照组均显著升高[(35.85±8.72)、(24.13±6.86)、(15.34±4.66)、(9.15±2.25)个比(6.31±1.49)个,P<0.05],A549细胞诱导HUVEC成管数量均随TWP浓度升高而显著降低(P<0.05)。结论TWP可能通过抑制PI3K/AKT信号通路激活,抑制肺腺癌A549细胞的增殖、迁移、血管生成行为,并诱导细胞凋亡。
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(0,20,40,80μmol/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,the migration 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 80μmol/L TWP groups increased significantly with the increase of culture time(P<0.05);the apoptosis rate of A549 cells in 20,40 and 80μmol/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 80μmol/L TWP groups 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.
作者
马春兰
张宝亮
刘晓明
MA Chunlan;ZHANG Baoliang;LIU Xiaoming(Department of Pharmacy,the Fifth People's Hospital of Qinghai,Xining,Qinghai 810007,China;Department of Breast Surgery,the Fifth People's Hospital of Qinghai,Xining,Qinghai 810007,China;Department of Stomatology,Affiliated Hospital of Qinghai University,Xining,Qinghai 810001,China)
出处
《安徽医药》
CAS
2022年第2期235-238,共4页
Anhui Medical and Pharmaceutical Journal
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
Adenocarcinoma,bronchiolo-alveolar
Tripterygium wilfordii polyglycosidium
Phosphatidylinositol 3-kinase
Protein kinase B
Migration
Angiogenesis
