Objective： Acute myeloid leukemia progressed from myelodysplastic syndrome （MDS/AML） is generally incurable with poor prognosis for complex karyotype including monosomy 7 （-7）. Qinghuang Powder （青黄, QHP）, whi...Objective： Acute myeloid leukemia progressed from myelodysplastic syndrome （MDS/AML） is generally incurable with poor prognosis for complex karyotype including monosomy 7 （-7）. Qinghuang Powder （青黄, QHP）, which includes Qing Dai （ Indigo naturalis） and Xiong Huang （realgar） in the formula, is effective in treating MDS or MDS/AML even with the unfavorable karyotype, and its therapeutic efficacy could be enhanced by increasing the Xiong huang content in the formula, while Xiong huang contains 〉 90% arsenic disulfide （As2S2）. F-36p cell line was established from a MDS/AML patient with complex karyotype including -7, and was in cytokine-dependent. The present study was to investigate the effects of As2S2 on F-36p cells. Methods： Cell proliferation was measured by an 3-（4,5-dimethylthiazol-2-yl）-2, 5-diphenyltetrazolium bromide （MTT） assay. Cell apoptosis was identified by Annexin V-staining. Cell viability was determined by a propidium iodide （PI） exclusion. Erythroid differentiation was evaluated by the expression of cell surface antigen CD235a （GpA）. Results： After treatment with As2S2 at concentrations of 0.5 to 16 p. mol/L for 72 h, As2S2 inhibited the proliferation of F-36p cells. The 50% inhibitory concentrations （IC50） of As2S2 against the proliferation of F-36p cells was 6 I~ mol/L. The apoptotic cells significantly increased in a dose-dependent mannar （P〈0.05）. The cell viabilities were significantly inhibited by As2S2 dose-dependent in a dose-dependent manner （P〈0.05）. Significant increases of CD235a-positive cells were concurrently observed （P〈0.05） also in a dose- dependent manner. Conclusions： As2S2 could inhibit proliferation and viability, induce apoptosis, and concurrently promote erythroid differentiation dose-dependently in F-36p cells. As2S2 can inhibit proliferation and viability, induce apoptosis, and concurrently promote erythroid differentiation in cytokine-dependent MDS-progressed human leukemia cell line F-36p with co展开更多
基金Supported in part by grants from Japan China Medical Association to Bo Yuan and XiaoMei Hu
文摘Objective： Acute myeloid leukemia progressed from myelodysplastic syndrome （MDS/AML） is generally incurable with poor prognosis for complex karyotype including monosomy 7 （-7）. Qinghuang Powder （青黄, QHP）, which includes Qing Dai （ Indigo naturalis） and Xiong Huang （realgar） in the formula, is effective in treating MDS or MDS/AML even with the unfavorable karyotype, and its therapeutic efficacy could be enhanced by increasing the Xiong huang content in the formula, while Xiong huang contains 〉 90% arsenic disulfide （As2S2）. F-36p cell line was established from a MDS/AML patient with complex karyotype including -7, and was in cytokine-dependent. The present study was to investigate the effects of As2S2 on F-36p cells. Methods： Cell proliferation was measured by an 3-（4,5-dimethylthiazol-2-yl）-2, 5-diphenyltetrazolium bromide （MTT） assay. Cell apoptosis was identified by Annexin V-staining. Cell viability was determined by a propidium iodide （PI） exclusion. Erythroid differentiation was evaluated by the expression of cell surface antigen CD235a （GpA）. Results： After treatment with As2S2 at concentrations of 0.5 to 16 p. mol/L for 72 h, As2S2 inhibited the proliferation of F-36p cells. The 50% inhibitory concentrations （IC50） of As2S2 against the proliferation of F-36p cells was 6 I~ mol/L. The apoptotic cells significantly increased in a dose-dependent mannar （P〈0.05）. The cell viabilities were significantly inhibited by As2S2 dose-dependent in a dose-dependent manner （P〈0.05）. Significant increases of CD235a-positive cells were concurrently observed （P〈0.05） also in a dose- dependent manner. Conclusions： As2S2 could inhibit proliferation and viability, induce apoptosis, and concurrently promote erythroid differentiation dose-dependently in F-36p cells. As2S2 can inhibit proliferation and viability, induce apoptosis, and concurrently promote erythroid differentiation in cytokine-dependent MDS-progressed human leukemia cell line F-36p with co
