中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2009年
10期
1308-1310,1313
,共4页
芬维A铵/药理学%宫颈肿瘤/药物疗法%内质网%细胞凋亡
芬維A銨/藥理學%宮頸腫瘤/藥物療法%內質網%細胞凋亡
분유A안/약이학%궁경종류/약물요법%내질망%세포조망
Fenretinide/PD%Cervix neoplasms/DT%Endoplasmic reticulum%Apoptosis
目的 探索芬维A胺(4-HPR)对宫颈癌细胞的抗肿瘤作用及其机制.方法 应用MTT法检测4-HPR对宫颈癌细胞的生长抑制作用.Annexin V-FITC和碘化丙锭(PI)双染检测细胞凋亡.用对氧化敏感的荧光染料DCFH-DA检测细胞内活性氧.Western blot检测Bcl-2和CHOP蛋白表达.结果 4-HPR以浓度依赖方式抑制宫颈癌HeLa细胞的生长,其IC50约为5μM.4-HPR以浓度依赖方式诱导HeLa细胞凋亡,同时伴随Bcl-2蛋白表达下调.4-HPR短暂处理能升高细胞内活性氧水平.4-HPR还激活内质网应激凋亡途径,表现以活性氧依赖方式升高CHOP蛋白表达.结论 4-HPR对宫颈癌具有抗肿瘤作用,其机制为诱导产生细胞内活性氧和内质网应激通路的激活.
目的 探索芬維A胺(4-HPR)對宮頸癌細胞的抗腫瘤作用及其機製.方法 應用MTT法檢測4-HPR對宮頸癌細胞的生長抑製作用.Annexin V-FITC和碘化丙錠(PI)雙染檢測細胞凋亡.用對氧化敏感的熒光染料DCFH-DA檢測細胞內活性氧.Western blot檢測Bcl-2和CHOP蛋白錶達.結果 4-HPR以濃度依賴方式抑製宮頸癌HeLa細胞的生長,其IC50約為5μM.4-HPR以濃度依賴方式誘導HeLa細胞凋亡,同時伴隨Bcl-2蛋白錶達下調.4-HPR短暫處理能升高細胞內活性氧水平.4-HPR還激活內質網應激凋亡途徑,錶現以活性氧依賴方式升高CHOP蛋白錶達.結論 4-HPR對宮頸癌具有抗腫瘤作用,其機製為誘導產生細胞內活性氧和內質網應激通路的激活.
목적 탐색분유A알(4-HPR)대궁경암세포적항종류작용급기궤제.방법 응용MTT법검측4-HPR대궁경암세포적생장억제작용.Annexin V-FITC화전화병정(PI)쌍염검측세포조망.용대양화민감적형광염료DCFH-DA검측세포내활성양.Western blot검측Bcl-2화CHOP단백표체.결과 4-HPR이농도의뢰방식억제궁경암HeLa세포적생장,기IC50약위5μM.4-HPR이농도의뢰방식유도HeLa세포조망,동시반수Bcl-2단백표체하조.4-HPR단잠처리능승고세포내활성양수평.4-HPR환격활내질망응격조망도경,표현이활성양의뢰방식승고CHOP단백표체.결론 4-HPR대궁경암구유항종류작용,기궤제위유도산생세포내활성양화내질망응격통로적격활.
Objective To explore anti-tumor effect and its cancer prevention mechanism of drug 4-HPR.Methods MIT assay was performed to evaluate the growth inhibition effect of cervical cancer cells by 4-HPR.Annexin V-FITC and propidinm iodide(PI)double staining was performed to detect apoptotic cells.Oxidation-sensitive fluorescent dye DCFH-DA Was used for detection of intracellular reactive oxygen species(ROS).Western blot was used to detect Bcl-2 and CHOP protein expression.Results 4-HPR inhibits the growth of cervical cancer HeLa cells in a dose-dependent manner,with the IC50 about 5μM.4-HPR induced apoptosis in HeLa cells in a dose-dependent manner,while reduce Bcl-2 protein expression.4-HPR promptly increased the level of intracellulal reactive oxygen species.4-HPR also activated endoplasmic reticulum stress associated apoptosis,increasing CHOP protein expression in a reactive oxygen species-dependent manner.Conclusion 4-HPR have anti-tumor effect on cervical cancer cells,the mechanisms are based on reactive oxygen species elevation and endoplasmic reticulum stress-activated pathway.