Arsenic Disulfide Induced Apoptosis and Concurrently Promoted Erythroid Differentiation in Cytokine-Dependent Myelodysplastic Syndrome-progressed Leukemia Cell Line F-36p with Complex Karyotype Including Monosomy 7

作     者：胡晓梅 Sachiko Tanaka Kenji Onda 袁博 Hiroo Toyoda 麻柔 刘峰 Toshihiko Hirano 

作者机构：Department of Clinical PharmacologySchool of PharmacyTokyo University of Pharmacy and Life Sciences National Therapeutic Center of Hematology of Traditional Chinese MedicineXiyuan HospitalChina Academy of Chinese Medical Sciences 

出 版 物：《Chinese Journal of Integrative Medicine》 (中国结合医学杂志（英文版）)

年 卷 期：2014年第20卷第5期

页      面：387-393页

核心收录：

学科分类：1007[医学-药学(可授医学、理学学位)] 1005[医学-中医学] 1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基　　金：Supported in part by grants from Japan China Medical Association to Bo Yuan and XiaoMei Hu 

主　　题：leukemia myelodysplastic syndromes arsenic disulfide karyotype F-36p apoptosis erythroid diffeerentiation 

摘      要：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 complex karyotype including -7