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目的:探讨草苁蓉苯丙素苷(PGBR)对肺癌细胞增殖的抑制作用及其可能机制。方法:采用MTT法观察PGBR对A549肺癌细胞增殖的影响,采用流式细胞术检测对A549细胞周期分布和细胞凋亡的影响,采用TUNEL染色法检测对A549细胞凋亡的影响,免疫细胞化学法检测凋亡相关蛋白p53,Fas,Bax,Bc1-2蛋白的表达。结果:PGBR可时间和浓度依赖性地抑制肺癌细胞增殖,200 mg.L-1 PGBR作用于A549细胞12,24,48 h时,抑制率分别为(20.4±2.1)%,(27.1±2.0)%,(30.7±2.2)%。PGBR改变肺癌细胞周期分布,使G0/G1期细胞由(45.3±4.1)%增至(57.4±4.0)%,表现出G0/G1期阻滞;同时诱导肺癌细胞凋亡,凋亡率由(2.4±0.90)%增至(7.8±1.2)%。PGBR明显增加p53和Fas表达,增加Bax表达和降低Bc1-2表达。结论:PGBR可通过诱导细胞周期阻滞和细胞凋亡而发挥抗肺癌作用。
Objective: To investigate the inhibitory effect of PGE on the proliferation of lung cancer cells and its possible mechanism. Methods: MTT assay was used to observe the effect of PGBR on the proliferation of A549 lung cancer cells. The effect of PGBR on the cell cycle distribution and apoptosis of A549 cells was detected by flow cytometry. The apoptosis of A549 cells was detected by TUNEL staining. Immunocytochemistry The expressions of p53, Fas, Bax and Bcl-2 proteins were detected by immunohistochemistry. RESULTS: PGBR inhibited the proliferation of lung cancer cells in a time and concentration-dependent manner. The inhibitory rates of PGBR at 20, 24 and 48 h were (20.4 ± 2.1)% and (27.1 ± 2.0) %, (30.7 ± 2.2)%. PGBR changed the cell cycle distribution of lung cancer, and increased the number of cells in G0 / G1 phase from (45.3 ± 4.1)% to (57.4 ± 4.0)%, and showed G0 / G1 phase arrest. 2.4 ± 0.90)% to (7.8 ± 1.2)%. PGBR significantly increased p53 and Fas expression, increased Bax expression and decreased Bcl-2 expression. Conclusion: PGBR can prevent lung cancer by inducing cell cycle arrest and apoptosis.