中华普通外科杂志
中華普通外科雜誌
중화보통외과잡지
CHINESE JOURNAL OF GENERAL SURGERY
2011年
3期
219-221
,共3页
秦建民%徐夏君%盛霞%李琦%殷佩浩%张敏%杨林%撒忠秋
秦建民%徐夏君%盛霞%李琦%慇珮浩%張敏%楊林%撒忠鞦
진건민%서하군%성하%리기%은패호%장민%양림%살충추
癌,肝细胞%马钱子碱%药物筛选试验,抗肿瘤
癌,肝細胞%馬錢子堿%藥物篩選試驗,抗腫瘤
암,간세포%마전자감%약물사선시험,항종류
Carcinoma,hepatocellular%Brucine%Drug screening assay,antitumor
目的 探讨马钱子碱抗肝细胞癌的作用及其机制.方法 体外培养人肝癌SMMC-7721细胞,加入不同浓度的马钱子碱(2.5～400μg/ml),细胞培养72 h,MTT法测定细胞生长抑制率.Western blotting和荧光定量RT-PCR技术分别测定培养24、48、72 h肝癌细胞PCNA、Cyclin D1、FAS基因mRNA和蛋白表达.结果 随着马钱子碱用量逐渐增加,对人肝癌细胞SMMC-7721生长抑制作用增强,马钱子碱用量为320 μg/ml时对肝癌细胞生长抑制率接近100%.马钱子碱作用肝癌细胞24 h与作用48 h相比,Fas蛋白和mRNA表达差异无统计学意义(分别F=2.547,1.582,均P＞0.05),作用72 h时差异有统计学意义(分别F=1.036,1.137,均P＜0.05);PCNA和Cyclin D1的mRNA和蛋白表达各时间点差异无统计学意义(PCNA分别F=3.612,2.174,3.029;Cyclin D1分别F=2.361,2.915,1.976,均P＞0.05).结论 马钱子碱抑制肝癌细胞生长,可能通过肝癌细胞FAS基因和蛋白表达增加,诱导肝癌细胞凋亡发挥抑制作用,而与PCNA和Cyclin D1作用无关.
目的 探討馬錢子堿抗肝細胞癌的作用及其機製.方法 體外培養人肝癌SMMC-7721細胞,加入不同濃度的馬錢子堿(2.5～400μg/ml),細胞培養72 h,MTT法測定細胞生長抑製率.Western blotting和熒光定量RT-PCR技術分彆測定培養24、48、72 h肝癌細胞PCNA、Cyclin D1、FAS基因mRNA和蛋白錶達.結果 隨著馬錢子堿用量逐漸增加,對人肝癌細胞SMMC-7721生長抑製作用增彊,馬錢子堿用量為320 μg/ml時對肝癌細胞生長抑製率接近100%.馬錢子堿作用肝癌細胞24 h與作用48 h相比,Fas蛋白和mRNA錶達差異無統計學意義(分彆F=2.547,1.582,均P＞0.05),作用72 h時差異有統計學意義(分彆F=1.036,1.137,均P＜0.05);PCNA和Cyclin D1的mRNA和蛋白錶達各時間點差異無統計學意義(PCNA分彆F=3.612,2.174,3.029;Cyclin D1分彆F=2.361,2.915,1.976,均P＞0.05).結論 馬錢子堿抑製肝癌細胞生長,可能通過肝癌細胞FAS基因和蛋白錶達增加,誘導肝癌細胞凋亡髮揮抑製作用,而與PCNA和Cyclin D1作用無關.
목적 탐토마전자감항간세포암적작용급기궤제.방법 체외배양인간암SMMC-7721세포,가입불동농도적마전자감(2.5～400μg/ml),세포배양72 h,MTT법측정세포생장억제솔.Western blotting화형광정량RT-PCR기술분별측정배양24、48、72 h간암세포PCNA、Cyclin D1、FAS기인mRNA화단백표체.결과 수착마전자감용량축점증가,대인간암세포SMMC-7721생장억제작용증강,마전자감용량위320 μg/ml시대간암세포생장억제솔접근100%.마전자감작용간암세포24 h여작용48 h상비,Fas단백화mRNA표체차이무통계학의의(분별F=2.547,1.582,균P＞0.05),작용72 h시차이유통계학의의(분별F=1.036,1.137,균P＜0.05);PCNA화Cyclin D1적mRNA화단백표체각시간점차이무통계학의의(PCNA분별F=3.612,2.174,3.029;Cyclin D1분별F=2.361,2.915,1.976,균P＞0.05).결론 마전자감억제간암세포생장,가능통과간암세포FAS기인화단백표체증가,유도간암세포조망발휘억제작용,이여PCNA화Cyclin D1작용무관.
Objective To study the effect of brucine on the growth of a hepatocellular carcinoma cell line in vitro. Methods Brucine was added into a liver cancer cell line of SMMC-7721 in vitro, at drug concentration of brucine from 2. 5 μg/ml to 400 μg/ml. The inhibition rate of cell growth was measured by MTT technique after the cells were cultured for 72 hours. The protein and mRNA expression of PCNA,cyclin D1 and FAS were respectively assayed with Western blotting and fluorescent quantitation RT-PCR techniques at 24, 48, 72 h. Results The inhibition rate of liver cancer cell was near 100% when the brucine concentration was at 320 μg/ml. The protein and mRNA expression of FAS were of no significant difference at 24 h vs 48 h ( seperately F = 2. 547,1. 582, all P ＞ 0. 05 ), and significant difference existed at 24 h vs 72 h( seperately F = 1. 036, 1. 137, all P ＜ 0. 05 ). The protein and mRNA expression of PCNA,Cyclin D1 were of no significant difference between various time period( seperately PCNA F = 3.612,2. 174,3.029;Cyclin D1 F=2.361,2.915,1.976,all P＞0.05). Conclusions Brucine inhibits the growth of liver cancer cells, by inducing increased apoptosis of the cells probably through FAS overexpression.
