南京医科大学学报（英文版）
南京醫科大學學報（英文版）
남경의과대학학보（영문판）
JOURNAL OF NANJING MEDICAL UNIVERSITY(ENGLISH EDITION)
2004年
6期
297-300
,共4页
肝癌%三氧化二砷%抗坏血酸%凋亡%caspase-3%ERKs信号蛋白
肝癌%三氧化二砷%抗壞血痠%凋亡%caspase-3%ERKs信號蛋白
간암%삼양화이신%항배혈산%조망%caspase-3%ERKs신호단백
hepatocarcinoma%arsenic trioxide%Ascorbic acid%apoptosis%caspase-3%extracellular-signal regulated kinases
目的:探讨抗干血酸(AA)对三氧化二砷(AT)诱导人肝癌细胞凋亡的协同效应,为改善三氧化二砷临床治疗人肝癌细胞提供理论基础.方法:体外培养人肝癌细胞株BEL-7402,用MTT和免疫印迹的方法分别评价AT和(或)AA对其生长抑制和胞内两个信号分子的影响.结果:微摩尔剂量的AT能抑制人肝癌细胞BEL-7402的异常生长,通过caspase-3的激活诱导其凋亡,并激活了ERKs信号蛋白,其作用有明显的剂量依赖性.AA对BEL-7402无明显的作用,但能有效的通过caspase-3而不是ERKs的激活促进AT对肝癌细胞的凋亡效应.结论:ERKs和caspase-3信号蛋白可能分别参与了砷剂诱导的人肝癌细胞促分化和凋亡效应,AT和AA对肝癌细胞的作用有协同性,他们通过caaspase-3而不是ERKs的激活进一步抑制了肝癌的生长,诱导其凋亡.
目的:探討抗榦血痠(AA)對三氧化二砷(AT)誘導人肝癌細胞凋亡的協同效應,為改善三氧化二砷臨床治療人肝癌細胞提供理論基礎.方法:體外培養人肝癌細胞株BEL-7402,用MTT和免疫印跡的方法分彆評價AT和(或)AA對其生長抑製和胞內兩箇信號分子的影響.結果:微摩爾劑量的AT能抑製人肝癌細胞BEL-7402的異常生長,通過caspase-3的激活誘導其凋亡,併激活瞭ERKs信號蛋白,其作用有明顯的劑量依賴性.AA對BEL-7402無明顯的作用,但能有效的通過caspase-3而不是ERKs的激活促進AT對肝癌細胞的凋亡效應.結論:ERKs和caspase-3信號蛋白可能分彆參與瞭砷劑誘導的人肝癌細胞促分化和凋亡效應,AT和AA對肝癌細胞的作用有協同性,他們通過caaspase-3而不是ERKs的激活進一步抑製瞭肝癌的生長,誘導其凋亡.
목적:탐토항간혈산(AA)대삼양화이신(AT)유도인간암세포조망적협동효응,위개선삼양화이신림상치료인간암세포제공이론기출.방법:체외배양인간암세포주BEL-7402,용MTT화면역인적적방법분별평개AT화(혹)AA대기생장억제화포내량개신호분자적영향.결과:미마이제량적AT능억제인간암세포BEL-7402적이상생장,통과caspase-3적격활유도기조망,병격활료ERKs신호단백,기작용유명현적제량의뢰성.AA대BEL-7402무명현적작용,단능유효적통과caspase-3이불시ERKs적격활촉진AT대간암세포적조망효응.결론:ERKs화caspase-3신호단백가능분별삼여료신제유도적인간암세포촉분화화조망효응,AT화AA대간암세포적작용유협동성,타문통과caaspase-3이불시ERKs적격활진일보억제료간암적생장,유도기조망.
Objective: To study synergistic effect with Ascorbic acid (AA) on arsenic trioxide inducing human Hepatocarcinoma cell apoptosis, and provide theoretical basis for promoting human Hepatocarcinoma cell apoptosis induced by arsenic trioxide(AT). Methods: Human Hepatocarcinoma cell line BEL-7402 being cultured in vitro, the effect of AT and (or) AA on its growth inhibition and its two intracellular signal molecules was evaluated separately using MTT and Western blot. Results: AT at a few μmol/L concentration could suppress abnormal proliferation of human hepatocarcinoma cells, and initiate their apoptosis by activation of caspase-3, and activate extracellular-signal regulated kinases (ERKs), which were dependent on the dosage of AT conspicuously. The effect of AA on BEL-7402 was not significant; However, AA could effectively enhance AT-induced hepatocarcinoma cell apoptosis and lesion severity through activation of caspase-3 but not ERKs. Conclusion: Caspase-3 and ERKs proteins could involve in arsenic-induced hepatocarcinoma cell apoptosis and differentiation respectively as intracellular signaling molecules; The effect between AT and AA on hepatocarcinoma is synergistic, which further inhibits cell growth and induces apoptosis in human hepatocarcinoma cells through activation of caspase-3 but not ERKs.
