中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2011年
10期
1668-1669
,共2页
祝葆华%张国平%李明意%王兰天%苑进凯
祝葆華%張國平%李明意%王蘭天%苑進凱
축보화%장국평%리명의%왕란천%원진개
癌,肝细胞%柴胡皂甙-d%p27%细胞周期
癌,肝細胞%柴鬍皂甙-d%p27%細胞週期
암,간세포%시호조대-d%p27%세포주기
Carcinoma,hepatocellular%Saikosaponins-d%p27%Cell cycle
目的 观察柴胡皂甙-d(SSd)对人肝癌HepG2细胞周期的阻滞作用及对其p27基因表达的影响.方法 常规培养人肝癌HepG2细胞至对数生长期,随机分为两组,实验组10 mg/L的SSd作用48 h,设空白对照；流式细胞术(FCM)检测细胞周期分布；逆转录-聚合酶链反应(RT-PCR)检测细胞p27基因mRNA表达；免疫组织化学SP法检测p27蛋白的表达.结果 实验组HepG2细胞G1期百分率为(69.43 ±3.01)％较对照组(62.83±2.72)％明显增加(P＜0.05),S期细胞百分率为(22.30±0.82)％较对照组(27.23±0.59)％明显减少(P＜0.01)；p27基因mRNA相对表达量(0.566 ±0.001)较对照组(0.335±0.000)明显增多(P＜0.05)；p27蛋白表达阳性率为(33.9±3.1)％较对照组(21.9±1.7)％亦明显增多(P＜0.01).结论 SSd可导致人肝癌HepG2细胞周期阻滞于G1期,其机制可能与上调p27基因表达有关.
目的 觀察柴鬍皂甙-d(SSd)對人肝癌HepG2細胞週期的阻滯作用及對其p27基因錶達的影響.方法 常規培養人肝癌HepG2細胞至對數生長期,隨機分為兩組,實驗組10 mg/L的SSd作用48 h,設空白對照；流式細胞術(FCM)檢測細胞週期分佈；逆轉錄-聚閤酶鏈反應(RT-PCR)檢測細胞p27基因mRNA錶達；免疫組織化學SP法檢測p27蛋白的錶達.結果 實驗組HepG2細胞G1期百分率為(69.43 ±3.01)％較對照組(62.83±2.72)％明顯增加(P＜0.05),S期細胞百分率為(22.30±0.82)％較對照組(27.23±0.59)％明顯減少(P＜0.01)；p27基因mRNA相對錶達量(0.566 ±0.001)較對照組(0.335±0.000)明顯增多(P＜0.05)；p27蛋白錶達暘性率為(33.9±3.1)％較對照組(21.9±1.7)％亦明顯增多(P＜0.01).結論 SSd可導緻人肝癌HepG2細胞週期阻滯于G1期,其機製可能與上調p27基因錶達有關.
목적 관찰시호조대-d(SSd)대인간암HepG2세포주기적조체작용급대기p27기인표체적영향.방법 상규배양인간암HepG2세포지대수생장기,수궤분위량조,실험조10 mg/L적SSd작용48 h,설공백대조；류식세포술(FCM)검측세포주기분포；역전록-취합매련반응(RT-PCR)검측세포p27기인mRNA표체；면역조직화학SP법검측p27단백적표체.결과 실험조HepG2세포G1기백분솔위(69.43 ±3.01)％교대조조(62.83±2.72)％명현증가(P＜0.05),S기세포백분솔위(22.30±0.82)％교대조조(27.23±0.59)％명현감소(P＜0.01)；p27기인mRNA상대표체량(0.566 ±0.001)교대조조(0.335±0.000)명현증다(P＜0.05)；p27단백표체양성솔위(33.9±3.1)％교대조조(21.9±1.7)％역명현증다(P＜0.01).결론 SSd가도치인간암HepG2세포주기조체우G1기,기궤제가능여상조p27기인표체유관.
Objective To observe the effect of Saikosaponins-d (SSd) on cell cycle arrest and p27 expression of HepG2 cells.Methods HepG2 cells were cultured and divided into two groups randomly.The cell cycle of HepG2 was determined by FCM,the expression level of p27 mRNA and protein was detected by using reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry respectively.Results The proportion of HepG2 cells in G1 phase (69.43 ± 3.01 ) ％ in experimental group was higher than that (62.83 ± 2.72 ) ％ in control group significantly ( P ＜ 0.05 ),but that in S phase (22.30 ±0.82)％ was fewer than that (27.23 ±0.59)％ in control group (P ＜0.01 ).The p27 mRNA expression level of HepG2 in experimental group (0.566 ±0.001 ) was higher than that (0.335 ±0.000)in control group (P ＜ 0.05),and the p27 protein expression level ( 33.9 ± 3.1 ) ％ was higher than that (21.9 ± 1.7)％ of control group (P ＜0.01 ).Conclusion SSd could up-regulate p27 mRNA and protein expression of HepG2 cells and resulted in cell cycle arrest in G1 phase.
