扶正抗癌方联合吉非替尼对肺癌A549细胞的影响及机制  

Effect of Fuzheng Kang'ai Recipe Combined Gefitinib on Lung Cancer A549 Cells and Its Mechanism Research

作　　者：杨小兵[1] 陈晓[1] 吴万垠[1] 龙顺钦[1] 陈世敏[1] 韩守威[1] 

机构地区：[1]广东省中医院肿瘤科,广州510120

出　　处：《中国中西医结合杂志》2016年第11期1340-1344,共5页Chinese Journal of Integrated Traditional and Western Medicine

基　　金：国家自然科学基金资助项目(No.81273965;81503507);广东省自然科学基金-博士启动项目(No.2015A030310245);广东省建设中医药强省科研课题(No.20141104)

摘　　要：目的观察扶正抗癌方联合吉非替尼对肺癌A549细胞生长、凋亡的影响,探讨其协同抗肿瘤的可能机制。方法应用MTT法检测扶正抗癌方(0.211、0.316、0.474、0.711、1.067、1.6、2.4、3.6 mg/m L)和吉非替尼(3.95、5.92、8.18、13.33、20、30、45、67.5!mol/L)对A549细胞增殖的影响;用流式细胞术观察对照组(完全培养液组)、中药组(扶正抗癌方,1.6 mg/m L)、西药组(吉非替尼,45!mol/L)、联合组(扶正抗癌方1.6 mg/m L+吉非替尼45!mol/L)A549细胞凋亡;用Western blot检测各组EGFR、p-EGFR、EZH2、PPAR-γ及P53蛋白表达。结果扶正抗癌方及吉非替尼均有抑制肿瘤细胞增殖作用。扶正抗癌方联合吉非替尼干预后细胞凋亡率为(12.6±4.5)%,明显高于扶正抗癌方(4.6±0.7)%及吉非替尼(7.8±2.7)%,差异有统计学意义(P<0.05)。与对照组比较,联合组p-EGFR、EZH2下调(P<0.05),PPAR-γ及P53蛋白上调(P<0.05),西药组及中药组EZH2下调(P<0.05),中药组PPAR-γ上调(P<0.05);与西药组比较,联合组p-EGFR下调(P<0.05),PPAR-γ上调(P<0.05);与中药组比较,联合组p-EGFR下调(P<0.05)。结论扶正抗癌方联合吉非替尼能显著抑制A549细胞的增殖生长,促使肿瘤细胞凋亡;其协同抗肿瘤活性的机制可能与下调p-EGFR、EZH2及上调PPAR-γ、P53蛋白有关。Objective To observe the effect of Fuzheng Kang＇ai Recipe （FKR） combined ge- fitinib on the proliferation and apoptosis of lung cancer A549 cells, and to study its potential synergistic mechanish with gefitinib. Methods The effects of FKR （0.211, 0.316, 0.474, 0.711, 1. 067, 1. 600, 2.400, 3.600 mg/mL） combined gefitinib （3.95, 5.92,8.18, 13.33, 20.00, 30.00,45.00,67.50 μmol/ L） on the proliferation of A549 cells were detected by MTT assay. The apoptosis of A549 cells in the con- trol group （complete culture medium）, FKR （1.6 mg/mL）, gefitinib （45 μmol/L）, and FKR plus gefitinib （ 1.6 mg/mL ＋45 μmol/L） were detected by flow cytometry （FCM）. Their expressions of epidermal growth factor receptor （EGFR）, phosphorylating epidermal growth factor receptor （p-EGFR）, enhancer of zeste homolog 2 （EZH2）, peroxisome proliferator-activated receptor-γ （PPAR-γ）, and P53 protein in A549 cells were detected by Western blot. Results Both FKR and gefitinib could inhibit the proliferation of A549 cells. The apoptotic rate was 12.6% ±4.5% in the FKR combined gefitinib group, obviously higher than that of the FKR group（4.6% ±0.7%） and the gefitinib group （7.8% ±2.7%）, showing statistical difference （P 〈0.05）. Compared with the control group, the expressions of p-EGFR and EZH2 were sig- nificantly down-regulated （P 〈0.05）, the expressions of PPAR-γ, and P53 protein were up-regulated in the FKR combined gefitinib group （P 〈0.05）; the expression of EZH2 was down-regulated in the gefitinibgroup and the FKR group （P 〈0.05）; the expression of PPAR-γ was up-regulated in the FKR group （P 〈 0.05 ）. Compared with the gefitinib group, the expression of p-EGFR was down-regulated, and the expres- sion of PPAR-γ was up-regulated in the FKR combined gefitinib group （both P 〈0.05）. Compared with the FKR group, the expression of p-EGFR was down-regulated in the FKR combined gefitinib group （P 〈 0.05）. Conclusions Combination of FKR and gef

关 键 词：扶正抗癌方 吉非替尼 肺癌 协同作用 

分 类 号：R734.2[医药卫生—肿瘤]