中国肿瘤临床（英文版）
中國腫瘤臨床（英文版）
중국종류림상（영문판）
CHINESE JOURNAL OF CLINICAL ONCOLOGY
2008年
1期
22-25
,共4页
李航宇%鞠培新%钟鑫平%Xinping Zhong%Jingang Liu
李航宇%鞠培新%鐘鑫平%Xinping Zhong%Jingang Liu
리항우%국배신%종흠평%Xinping Zhong%Jingang Liu
三氧化二砷%肝癌%MTT法%Western blot法
三氧化二砷%肝癌%MTT法%Western blot法
삼양화이신%간암%MTT법%Western blot법
arsenic trioxide%hepatic cancer%MTT assay%Western blot.
目的:探讨三氧化二砷(As2O3)诱导人肝癌细胞株HepG2凋亡的作用及机制.方法:采用MTT法观察不同浓度的As2O3对人类肝癌细胞株HepG2细胞生长的抑制作用:以流式细胞术观察细胞的凋亡率;以Western blot法检测JNK、p-JNK、caspase-3及PARP蛋白在As2O3作用下及SP600125阻断JNK信号转导通路情况下的表达.结果:As2O3均对体外生长的肝癌细胞HepG2具有明显抑制作用,并可诱导细胞凋亡.Western Bloting结果显示,As2O3诱导肝癌细胞HepG2凋亡伴随着Caspase-3和PARP的活化;As2O3作用于HepG2细胞10min后p-JNK蛋白表达开始增加,20分钟达到高峰,30分钟开始减少,总JNK蛋白的含量无明显改变,JNK的激活早于细胞凋亡:用SP600125预处理HepG2细胞株后,可以明显减少Caspase-3和PARP的活化.结论:As2O3可以体外通过诱导细胞凋亡抑制肝癌细胞株HepG2的增殖,细胞凋亡通过Caspase-3途径实现.JNK信号转导通路参与了As2O3诱导的HepG2凋亡反应,并位于Caspase-3的上游.
目的:探討三氧化二砷(As2O3)誘導人肝癌細胞株HepG2凋亡的作用及機製.方法:採用MTT法觀察不同濃度的As2O3對人類肝癌細胞株HepG2細胞生長的抑製作用:以流式細胞術觀察細胞的凋亡率;以Western blot法檢測JNK、p-JNK、caspase-3及PARP蛋白在As2O3作用下及SP600125阻斷JNK信號轉導通路情況下的錶達.結果:As2O3均對體外生長的肝癌細胞HepG2具有明顯抑製作用,併可誘導細胞凋亡.Western Bloting結果顯示,As2O3誘導肝癌細胞HepG2凋亡伴隨著Caspase-3和PARP的活化;As2O3作用于HepG2細胞10min後p-JNK蛋白錶達開始增加,20分鐘達到高峰,30分鐘開始減少,總JNK蛋白的含量無明顯改變,JNK的激活早于細胞凋亡:用SP600125預處理HepG2細胞株後,可以明顯減少Caspase-3和PARP的活化.結論:As2O3可以體外通過誘導細胞凋亡抑製肝癌細胞株HepG2的增殖,細胞凋亡通過Caspase-3途徑實現.JNK信號轉導通路參與瞭As2O3誘導的HepG2凋亡反應,併位于Caspase-3的上遊.
목적:탐토삼양화이신(As2O3)유도인간암세포주HepG2조망적작용급궤제.방법:채용MTT법관찰불동농도적As2O3대인류간암세포주HepG2세포생장적억제작용:이류식세포술관찰세포적조망솔;이Western blot법검측JNK、p-JNK、caspase-3급PARP단백재As2O3작용하급SP600125조단JNK신호전도통로정황하적표체.결과:As2O3균대체외생장적간암세포HepG2구유명현억제작용,병가유도세포조망.Western Bloting결과현시,As2O3유도간암세포HepG2조망반수착Caspase-3화PARP적활화;As2O3작용우HepG2세포10min후p-JNK단백표체개시증가,20분종체도고봉,30분종개시감소,총JNK단백적함량무명현개변,JNK적격활조우세포조망:용SP600125예처리HepG2세포주후,가이명현감소Caspase-3화PARP적활화.결론:As2O3가이체외통과유도세포조망억제간암세포주HepG2적증식,세포조망통과Caspase-3도경실현.JNK신호전도통로삼여료As2O3유도적HepG2조망반응,병위우Caspase-3적상유.
OBJECTIVE To study the anti-tumor effect of arsenic trioxide on the HepG2human hepatocellular carcinoma cell line,and to explore its mechanism of action.METHODS The MTT assay was used to determine the inhibitory effect of As2O3 on HepG,cells at various As2O3 concentrations.The expression of p-JNK,caspase-3 and PARP was detected by Western blots.RESULTS As2O3markedly inhibited the growth of the HepG2 cells and induced apoptosis.The results of Western blol analysis showed that the As2O3-induced apoptosis was accompanied by caspase-3 and PARP activation.p-JNK was detected at 10 min following As2O3treatment,and preceded to peak at 20 min,and decreased by 30 min.The total protein content did not obviously change.The activation of JNK occurred prior tO cell apoptosis.SP600125,a JNK inhibitor,suppressed the As2O3-induced activation of Gaspase-3 and PARP cleavage.CONCLUSION As2O3 inhibits the proliferation of human HepG2hepatocellular carcinoma cells by inducing apoptosis in vitro.As2O3-induced apoptosis is accessed through the caspase-3 pathway.The JNK signal-transduction pathway and caspase-3 are involved upstream in the As2O3-induced HepG2apoptotic response.
