中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2015年
1期
21-23
,共3页
代荣钦%秦涛%秦秉玉%郭志松%张文筱%史源%王海波
代榮欽%秦濤%秦秉玉%郭誌鬆%張文篠%史源%王海波
대영흠%진도%진병옥%곽지송%장문소%사원%왕해파
丙戊酸钠%胰腺肿瘤%细胞株,肿瘤%细胞凋亡%Survivin基因
丙戊痠鈉%胰腺腫瘤%細胞株,腫瘤%細胞凋亡%Survivin基因
병무산납%이선종류%세포주,종류%세포조망%Survivin기인
Sodium valproate%Pancreatic neoplasms%Cell line,tumor%Apoptosis%Survivin gene
目的 观察丙戊酸钠(VPA)对胰腺癌细胞株SW1990增殖、凋亡的影响,探讨丙戊酸钠诱导SW1990凋亡的机制.方法 应用1、2、3、4、5 mmol/L的丙戊酸钠干预SW1990细胞,以未干预的细胞作为对照组.采用噻唑蓝(MTT)法检测细胞增殖;取3 mmol/L丙戊酸钠干预SW1990细胞24、48、72 h,流式细胞仪检测细胞凋亡;实时定量聚合酶链反应(Real-time PCR)法检测SurvivinmRNA的表达.结果 丙戊酸钠对SW1990细胞有明显的生长抑制作用,呈现明显的浓度依赖性和时间依赖性,不同浓度组、不同时间组间生长抑制率差异有统计学意义(P＜0.05).3 mmol/L丙戊酸钠干预SW1990细胞不同时间的凋亡率分别为(15.79 ±2.18)％、(26.73±2.36)％、(38.74±1.83)％,与对照组早期凋亡率[(2.99±0.87)％]比较,不同时间比较差异有统计学意义(P＜0.05).未经丙戊酸钠干预的SW1990细胞高表达Survivin基因(5.152±1.835),在经3 mmol/L丙戊酸钠干预24、48、72 h后,Survivin基因的表达水平分别为3.977±1.531、2.639±1.017、1.034±0.239,随药物干预时间的延长Survivin基因的表达水平逐渐下降,差异有统计学意义(P＜0.05).结论 丙戊酸钠可抑制胰腺癌细胞SW1990的增殖、诱导凋亡,其机制可能与激活线粒体内源性凋亡途径,下调Survivin基因有关.
目的 觀察丙戊痠鈉(VPA)對胰腺癌細胞株SW1990增殖、凋亡的影響,探討丙戊痠鈉誘導SW1990凋亡的機製.方法 應用1、2、3、4、5 mmol/L的丙戊痠鈉榦預SW1990細胞,以未榦預的細胞作為對照組.採用噻唑藍(MTT)法檢測細胞增殖;取3 mmol/L丙戊痠鈉榦預SW1990細胞24、48、72 h,流式細胞儀檢測細胞凋亡;實時定量聚閤酶鏈反應(Real-time PCR)法檢測SurvivinmRNA的錶達.結果 丙戊痠鈉對SW1990細胞有明顯的生長抑製作用,呈現明顯的濃度依賴性和時間依賴性,不同濃度組、不同時間組間生長抑製率差異有統計學意義(P＜0.05).3 mmol/L丙戊痠鈉榦預SW1990細胞不同時間的凋亡率分彆為(15.79 ±2.18)％、(26.73±2.36)％、(38.74±1.83)％,與對照組早期凋亡率[(2.99±0.87)％]比較,不同時間比較差異有統計學意義(P＜0.05).未經丙戊痠鈉榦預的SW1990細胞高錶達Survivin基因(5.152±1.835),在經3 mmol/L丙戊痠鈉榦預24、48、72 h後,Survivin基因的錶達水平分彆為3.977±1.531、2.639±1.017、1.034±0.239,隨藥物榦預時間的延長Survivin基因的錶達水平逐漸下降,差異有統計學意義(P＜0.05).結論 丙戊痠鈉可抑製胰腺癌細胞SW1990的增殖、誘導凋亡,其機製可能與激活線粒體內源性凋亡途徑,下調Survivin基因有關.
목적 관찰병무산납(VPA)대이선암세포주SW1990증식、조망적영향,탐토병무산납유도SW1990조망적궤제.방법 응용1、2、3、4、5 mmol/L적병무산납간예SW1990세포,이미간예적세포작위대조조.채용새서람(MTT)법검측세포증식;취3 mmol/L병무산납간예SW1990세포24、48、72 h,류식세포의검측세포조망;실시정량취합매련반응(Real-time PCR)법검측SurvivinmRNA적표체.결과 병무산납대SW1990세포유명현적생장억제작용,정현명현적농도의뢰성화시간의뢰성,불동농도조、불동시간조간생장억제솔차이유통계학의의(P＜0.05).3 mmol/L병무산납간예SW1990세포불동시간적조망솔분별위(15.79 ±2.18)％、(26.73±2.36)％、(38.74±1.83)％,여대조조조기조망솔[(2.99±0.87)％]비교,불동시간비교차이유통계학의의(P＜0.05).미경병무산납간예적SW1990세포고표체Survivin기인(5.152±1.835),재경3 mmol/L병무산납간예24、48、72 h후,Survivin기인적표체수평분별위3.977±1.531、2.639±1.017、1.034±0.239,수약물간예시간적연장Survivin기인적표체수평축점하강,차이유통계학의의(P＜0.05).결론 병무산납가억제이선암세포SW1990적증식、유도조망,기궤제가능여격활선립체내원성조망도경,하조Survivin기인유관.
Objective To investigate the effect of sodium valproate on proliferation and apoptosis of pancreatic cell line SW1990 in vitro and explore possible chanisms of sodium valproate' s effect on SW1990.Methods SW1990 cells were treated with 1,2,3,4,5 mmol/L sodium valproate,and cells without sodium valproate treatment were considered as control group.The cell proliferation was determined by methyl thiazol tetrazolium (MTT) assay.Apoptosis was detected by flow cytometry.Survivin mRNA was measured by real-time quantitative polymerase chain reaction (Real-time PCR).Results Sodium valproate could significantly inhibited the growth of SW1990 cells and showed significant concentration-dependent and time-dependent.The difference among these groups were statistically significant (P ＜0.05).Apoptosis rates in the different time groups of SW1990 treated by 3 mmol/L sodium valproate were respectively (15.79 ±2.18)％,(26.73 ±2.36)％,(38.74 ± 1.83)％.The apoptosis rate of control group [(2.99 ± 0.87)％] Compared with statistically significant difference among the different time groups (P ＜0.05).The high expression of Survivin gene in SW1990 cells without valproate intervention was 5.152 ± 1.835,after 3 mmol/L valproate intervention with 24,48,and 72 h,the expression of the Survivin gene were respectively 3.977 ± 1.531,2.639 ± 1.017,1.034 ± 0.239.With the extension of time of drug intervention,Survivin gene expression gradually decreased,the difference was statistically significant (P ＜ 0.05).Conclusion Sodium valproate can inhibit the proliferation of pancreatic cancer cell line SW1990 and induce apoptosis.The mechanism may depend on activation of the mitochondrial pathway of apoptosis and down-regulation of Survivin gene.
