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目的:探讨水杨酸(salicylic acid,SA)对人肝癌HepG2细胞体外生长的影响。方法:利用MTT法测定SA对HepG2细胞存活性的作用;利用EdU法检测SA对HepG2细胞增殖活性的影响;利用流式细胞分析法测定SA诱导的HepG2细胞周期进程和凋亡。结果:SA显著且呈浓度依赖的降低人肝癌HepG2细胞的存活率,其半数抑制浓度(IC50)为(8.92±0.45)mmol/L;EdU分析显示,SA作用24hr,EdU掺入的红色荧光强度明显减弱,降低了HepG2细胞的增殖活性;FCM分析显示,与对照比较,SA诱导HepG2细胞周期阻滞于G0/G1期(65.5%±1.21%vs.34.3%±0.89%,P<0.05),S期细胞占比明显降低(24.2%±0.89%vs.44.0%±0.64%,P<0.05),以及增加了HepG2细胞的凋亡率(24.9%±0.32%vs.2.3%±0.11%,P<0.05)。结论:SA诱导HepG2细胞周期阻滞,降低细胞增殖活性,促进细胞凋亡,从而抑制HepG2细胞的生长。
Objective: To investigate the effect of salicylic acid (SA) on the growth of human hepatocellular carcinoma HepG2 cells in vitro. Methods: The effect of SA on the viability of HepG2 cells was determined by MTT assay. The effect of SA on the proliferation of HepG2 cells was detected by EdU assay. The cell cycle progression and apoptosis of HepG2 cells were detected by flow cytometry. Results: SA significantly and in a concentration-dependent manner reduced the survival rate of HepG2 cells, and the IC50 was (8.92 ± 0.45) mmol / L. EdU analysis showed that the red fluorescent intensity (P <0.05). Compared with the control group, SA induced HepG2 cell cycle arrest in G0 / G1 phase (65.5% ± 1.21% vs.34.3% ± 0.89%, P <0.05), and significantly decreased the proliferation of HepG2 cells (24.2% ± 0.89% vs.44.0% ± 0.64%, P <0.05), and increased the apoptosis rate of HepG2 cells (24.9% ± 0.32% vs.2.3% ± 0.11%, P <0.05). Conclusion: SA induces HepG2 cell cycle arrest, decreases cell proliferation, promotes apoptosis and inhibits the growth of HepG2 cells.