摘要
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: Salicylic acid ( SA) and its derivatives have been shown to induce apoptosis in a variety of cancer cells. The aim of this study is to investigate influence of SA on human hepatic cancer HepG2 cells growth in-vitro. Methods:MTT assay was used to determine the effect of SA on viability of HepG2 cells, EdU assay was used to detect the impact of SA on the proliferation activity of HepG2 cells, and the cell cycle progress altered and apoptosis of HepG2 cells induced by SA were determined using flow cytometry ( FCM) . Results:SA reduced significantly viability of hepatic cancer HepG2 cells in a concentration-dependent manner and had an IC50 value of (8. 92 ± 0. 45)mmol/L;EdU assay showed that the red fluorescence produced by incorporation of EdU decreased in HepG2 cells treated with SA for 24hr, thereby depress-ing the proliferation activity of HepG2 cells;FCM assay showed that compared to control, SA induced obviously cell cycle G0/G1-phase arrest ( 65. 5% ± 1. 21% vs. 34. 3% ± 0. 89%, P 〈0. 05 ) and delayed in entering S phase 24. 2% ± 0. 89% vs. 44. 0% ± 0. 64%, P〈0. 05), and promoted apoptosis in HepG2 cells(24. 9% ± 0. 32% vs. 2. 3% ± 0. 11%, P〈0. 05). Conclusion:SA would inhibits the growth of HepG2 cells by altering cell cycle progress, depressing prolifera-tion activity and promoting cell apoptosis.
出处
《肿瘤预防与治疗》
2014年第3期126-129,共4页
Journal of Cancer Control And Treatment
基金
基金来源:川干研2012-504