肿瘤预防与治疗
腫瘤預防與治療
종류예방여치료
JOURNAL OF CANCER CONTROL AND TREATMENT
2014年
3期
126-129
,共4页
水杨酸%人肝癌HepG2细胞株%细胞周期%凋亡
水楊痠%人肝癌HepG2細胞株%細胞週期%凋亡
수양산%인간암HepG2세포주%세포주기%조망
Salicylic Acid%Human Hepatoma HepG2 Cell Line%Cell Cycle%Apoptosis
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。
目的：探討水楊痠( salicylic acid, SA)對人肝癌HepG2細胞體外生長的影響。方法：利用MTT法測定SA對HepG2細胞存活性的作用；利用EdU法檢測SA對HepG2細胞增殖活性的影響；利用流式細胞分析法測定SA誘導的HepG2細胞週期進程和凋亡。結果：SA顯著且呈濃度依賴的降低人肝癌HepG2細胞的存活率,其半數抑製濃度(IC50)為(8．92±0．45)mmol/L；EdU分析顯示,SA作用24hr,EdU摻入的紅色熒光彊度明顯減弱,降低瞭HepG2細胞的增殖活性；FCM分析顯示,與對照比較,SA誘導HepG2細胞週期阻滯于G0/G1期(65．5%±1．21%vs.34．3%±0．89%, P<0．05),S期細胞佔比明顯降低(24．2%±0．89% vs.44．0%±0．64%, P<0．05),以及增加瞭HepG2細胞的凋亡率(24．9%±0．32% vs.2．3%±0．11%, P<0．05)。結論：SA誘導HepG2細胞週期阻滯,降低細胞增殖活性,促進細胞凋亡,從而抑製HepG2細胞的生長。
목적：탐토수양산( salicylic acid, SA)대인간암HepG2세포체외생장적영향。방법：이용MTT법측정SA대HepG2세포존활성적작용；이용EdU법검측SA대HepG2세포증식활성적영향；이용류식세포분석법측정SA유도적HepG2세포주기진정화조망。결과：SA현저차정농도의뢰적강저인간암HepG2세포적존활솔,기반수억제농도(IC50)위(8．92±0．45)mmol/L；EdU분석현시,SA작용24hr,EdU참입적홍색형광강도명현감약,강저료HepG2세포적증식활성；FCM분석현시,여대조비교,SA유도HepG2세포주기조체우G0/G1기(65．5%±1．21%vs.34．3%±0．89%, P<0．05),S기세포점비명현강저(24．2%±0．89% vs.44．0%±0．64%, P<0．05),이급증가료HepG2세포적조망솔(24．9%±0．32% vs.2．3%±0．11%, P<0．05)。결론：SA유도HepG2세포주기조체,강저세포증식활성,촉진세포조망,종이억제HepG2세포적생장。
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.
