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目的研究胸腺肽α1诱导肺癌A549细胞凋亡的抗肿瘤机制。方法用不同浓度的胸腺肽α1(0,50,100 mg·L~(-1))处理A549细胞。24~72 h后,用MTT法检测细胞的生长活力。于48 h用流式细胞仪检测细胞的凋亡情况,用western blot检测凋亡相关蛋白caspase-3、Bcl-2、Bax的变化,分析胸腺肽α1对p-AKT/AKT途径的影响。结果 0 mg·L~(-1)胸腺肽α1组的72 h的细胞抑制率为0%,细胞凋亡率为(0.80±0.07)%,caspase-3为1.00±0.00,Bax为1.00±0.00,bcl-2为1.00±0.00,p-AKT抑制程度为0%;50 mg·L~(-1)胸腺肽α1组72 h的细胞抑制率为(23.51±3.44)%,细胞凋亡率为(5.36±1.07)%,caspase-3为3.74±0.56,Bax为4.11±0.82,Bcl-2为0.52±0.13,p-AKT抑制程度为(24.17±8.71)%;100 mg·L~(-1)胸腺肽α1组72 h的细胞抑制率为(31.90±5.04)%,细胞凋亡率为(10.00±2.97)%,caspase-3为3.74±0.56,Bax为4.11±0.82,Bcl-2为0.52±0.13,p-AKT抑制程度为(49.21±12.45)%。50、100 mg·L~(-1)胸腺肽α1组的细胞抑制率、细胞凋亡率、caspase-3、Bcl-2及Bax、p-AKT水平与0 mg·L~(-1)组相比,差异有统计学意义(P<0.05)。结论胸腺肽α1可以通过抑制AKT通路和抑制肺癌A549细胞增殖,诱导细胞凋亡发挥抗肿瘤作用。
Objective To study the anti-tumor mechanism of thymosin α1 inducing apoptosis of lung cancer A549 cells. Methods A549 cells were treated with different concentrations of thymosin α1 (0, 50, 100 mg · L -1). After 24 ~ 72 h, the cell viability was detected by MTT assay. The apoptosis of cells was detected by flow cytometry at 48 h. The changes of apoptosis related proteins caspase-3, Bcl-2 and Bax were detected by western blot, and the effect of thymosin α1 on p-AKT / AKT pathway was analyzed. Results Thymosin α1 in 0 mg · L -1 group had a cell inhibitory rate of 0% at 72 h, apoptosis rate of (0.80 ± 0.07)%, caspase-3 of 1.00 ± 0.00, Bax of 1.00 ± 0.00, The inhibition rate of bcl-2 was 1.00 ± 0.00 and the inhibition rate of p-AKT was 0%. The inhibition rate of thymosin α1 group (50 mg · L -1) for 72 h was (23.51 ± 3.44)% and the apoptosis rate was ± 1.07)%, caspase-3 was 3.74 ± 0.56, Bax was 4.11 ± 0.82, Bcl-2 was 0.52 ± 0.13 and the inhibition of p-AKT was (24.17 ± 8.71)%. The cell apoptosis rate in the α1 group was (31.90 ± 5.04)% at 72 h, the apoptotic rate was (10.00 ± 2.97)%, the caspase-3 was 3.74 ± 0.56, the Bax was 4.11 ± 0.82 and the Bcl-2 was 0.52 ± 0.13, The inhibition of p-AKT was (49.21 ± 12.45)%. The cell inhibitory rate, apoptosis rate, caspase-3, Bcl-2, Bax and p-AKT levels in 50,100 mg · L -1 thymosin α1 group were significantly higher than those in 0 mg · L -1 group The difference was statistically significant (P <0.05). Conclusion Thymosin α1 can exert antitumor effect by inhibiting AKT pathway and inhibiting the proliferation of lung cancer A549 cells and inducing apoptosis.