中华临床医师杂志（电子版）
中華臨床醫師雜誌（電子版）
중화림상의사잡지（전자판）
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2013年
23期
10793-10797
,共5页
二甲双胍%吉西他滨%胰腺肿瘤%凋亡
二甲雙胍%吉西他濱%胰腺腫瘤%凋亡
이갑쌍고%길서타빈%이선종류%조망
Metformin%Gemcitabine%Pancreatic neoplasms%Apoptosis
目的：探讨二甲双胍（Met）联合吉西他滨（GEM）对人胰腺癌细胞株 CFPAC-1的协同抑制作用及可能机制。方法以浓度为20 mmol/L的二甲双胍联合低浓度（5μmol/L）的吉西他滨处理对数生长期的人胰腺癌细胞株CFPAC-1，应用CCK-8法检测细胞的增殖抑制率；AnnexinⅤ/PI双染法检测细胞早期凋亡情况；RT-PCR检测细胞凋亡因子Bcl-xl、Bax、survivin、caspase-3的mRNA表达水平；免疫印迹法（Western Blot）检测凋亡蛋白Bcl-xl、Bax、survivin、caspase-3的表达水平。结果 Met和GEM都能有效地抑制人胰腺癌CFPAC-1细胞增殖，二者联合作用后抑制效应显著增强。Met组作用CFPAC-1细胞48 h后细胞早期凋亡为（24.53±2.18）%，GEM组为（22.37±1.61）%，联合组为（52.07±2.81）%。Met组、GEM组及联合组Bcl-xl、survivin mRNA及蛋白表达下调，Bax、caspase-3 mRNA及蛋白表达上调，各组与对照组、联合组与单药组相比均有统计学意义（P＜0.05）。结论二甲双胍联合吉西他滨对人胰腺癌细胞株CFPAC-1增殖具有协同抑制作用，其机制可能是通过促进细胞凋亡而发挥作用。
目的：探討二甲雙胍（Met）聯閤吉西他濱（GEM）對人胰腺癌細胞株 CFPAC-1的協同抑製作用及可能機製。方法以濃度為20 mmol/L的二甲雙胍聯閤低濃度（5μmol/L）的吉西他濱處理對數生長期的人胰腺癌細胞株CFPAC-1，應用CCK-8法檢測細胞的增殖抑製率；AnnexinⅤ/PI雙染法檢測細胞早期凋亡情況；RT-PCR檢測細胞凋亡因子Bcl-xl、Bax、survivin、caspase-3的mRNA錶達水平；免疫印跡法（Western Blot）檢測凋亡蛋白Bcl-xl、Bax、survivin、caspase-3的錶達水平。結果 Met和GEM都能有效地抑製人胰腺癌CFPAC-1細胞增殖，二者聯閤作用後抑製效應顯著增彊。Met組作用CFPAC-1細胞48 h後細胞早期凋亡為（24.53±2.18）%，GEM組為（22.37±1.61）%，聯閤組為（52.07±2.81）%。Met組、GEM組及聯閤組Bcl-xl、survivin mRNA及蛋白錶達下調，Bax、caspase-3 mRNA及蛋白錶達上調，各組與對照組、聯閤組與單藥組相比均有統計學意義（P＜0.05）。結論二甲雙胍聯閤吉西他濱對人胰腺癌細胞株CFPAC-1增殖具有協同抑製作用，其機製可能是通過促進細胞凋亡而髮揮作用。
목적：탐토이갑쌍고（Met）연합길서타빈（GEM）대인이선암세포주 CFPAC-1적협동억제작용급가능궤제。방법이농도위20 mmol/L적이갑쌍고연합저농도（5μmol/L）적길서타빈처리대수생장기적인이선암세포주CFPAC-1，응용CCK-8법검측세포적증식억제솔；AnnexinⅤ/PI쌍염법검측세포조기조망정황；RT-PCR검측세포조망인자Bcl-xl、Bax、survivin、caspase-3적mRNA표체수평；면역인적법（Western Blot）검측조망단백Bcl-xl、Bax、survivin、caspase-3적표체수평。결과 Met화GEM도능유효지억제인이선암CFPAC-1세포증식，이자연합작용후억제효응현저증강。Met조작용CFPAC-1세포48 h후세포조기조망위（24.53±2.18）%，GEM조위（22.37±1.61）%，연합조위（52.07±2.81）%。Met조、GEM조급연합조Bcl-xl、survivin mRNA급단백표체하조，Bax、caspase-3 mRNA급단백표체상조，각조여대조조、연합조여단약조상비균유통계학의의（P＜0.05）。결론이갑쌍고연합길서타빈대인이선암세포주CFPAC-1증식구유협동억제작용，기궤제가능시통과촉진세포조망이발휘작용。
Objective To investigate the effect and mechanism of metformin (Met) in combination with gemcitabine (GEM) on human pancreatic cancer cell line CFPAC-1. Methods THD, GEM, were tested alone and in combination for their abilities to inhibit CFPAC-1 cell lines proliferation by CCK-8. The early apoptosis of CFPAC-1 cell lines were detected by AnnexinⅤ/PI double staining method, and the expression of Bcl-xl, Bax, survivin and caspase-3 mRNA were detected by Semi-quantitative RT-PCR. In addition, the content of Bcl-xl, Bax, survivin and caspase-3 proteins were evaluated by Western Blot. Results The CFPAC-1 cell's proliferation could be effectively inhibited by Met or GEM; and the inhibition effect were more significantly while treated by Met combinated with GEM. The early stage apoptosis rate of CFPAC-1 cells was (24.53±2.18)% when they were treated with 20 mmol/L Met at 48 hr, and was (22.37±1.61)% when treated with 5 μmol/L of GEM, and was (52.07±2.81)% when Met combined with GEM. The expression of Bcl-xl, survivin mRNA and proteins were down-regulated, and Bax, caspase-3 mRNA and proteins levels were up-regulated in either Met, GEM or combination group. Comparisons of treated groups and control group have significant difference (P<0.05) and comparisons of combination groups and single drug group have also significant difference (P<0.05). Conclusions Metformin could obviously inhibit pancreatic cancer cell line CFPAC-1 proliferation in coordination with Gemcitabine.Its major mechanisms maybe promote apoptosis of cells.
