摘要
目的初步研究三氧化二砷（As2O3）作为急性早幼粒细胞性白血病（acute promyelocytic leukemia，APL）的治疗剂和环境污染物的毒副作用。方法用As2O3作用于293t细胞和HeLa细胞不同时间后，用流式细胞仪、Hoechst33258染色、形态学和超微结构观察检测细胞凋亡和增殖；检测293t细胞增殖用细胞记数板连续记数6天。结果3-5μmol／L As2O3作用24h可诱发HeLa细胞发生凋亡，而293t则不发生明显的凋亡。低浓度As2O3（〈2wnol／L）可抑制293t细胞增殖。结论不同浓度的As2O3对HeLa细胞和293t细胞的增殖和凋亡作用不同。
Objective To study the toxic mechanism of arsenic trioxide （As2 O3 ） both as a therapeutical agent for acute promyelocytic leukemia （APL） and an environmental pollutant.Methods 293t cells （a human embryoic kidney cell line） and Hela cells （a human cervical cancer cell line） were treated with different final concentrations of As2O3 for different hours. For apoptosis assays, flow cytometry, Hoechst33258 staining and cell morphological changes were used, and uhrastructure were observed. For proliferation assay, 293t cells were counted for continuous 6 days with a hemacytometer.Results When treated with 3 - 5μmaol/L As2 O3 for 24h, HeLa cells underwent conspicuous apoptosis,but 293t cells did not undergo obvious apoptosis.293t treated with 3 - 5μmol/L AS2O3 for 48- 72h experienced apparent apoptosis, low final concentrations of As2O3 （ 〈 2μmol/ L） inhibited proliferation of 293t cells. Conclusion Different final concentrations of As2 O3 play different roles in the proliferation and apoptosis of 293t and HeLa cells.
出处
《哈尔滨医科大学学报》
CAS
北大核心
2006年第2期116-120,共5页
Journal of Harbin Medical University
关键词
三氧化二砷
增殖
凋亡
arsenic trioxide
proliferation
apoptosis
