title: [Mechanism of Fas/FasL signal transduction pathway in K562 cell apoptosis induced by diallyl disulfide].
abstract: The aim of this study was to investigate the effect of diallyl disulfide (DADS) on the apoptosis of K562 cells and to explore the mechanism of K562 apoptosis induced by DADS. The K562 cells were treated with different concentrations of DADS for 24, 48 and 72 hours. The concentrations of DADS were as follows: 0 (control group), 10, 20, 40 and 80 mg/L. The morphologic changes of leukemia K562 cells treated with DADS were observed by Hoechst33 258 staining. The apoptosis of K562 cells treated with different concentrations of DADS for 24, 48 and 72 hours was analyzed by flow cytometry. The mRNA expression changes of Fas and FasL were detected by reverse transcription-polymerase chain reaction (RT-PCR) after K562 cells were treated with different concentrations of DADS for 48 hours. The results indicated that the characteristics of apoptosis in K562 cells induced by DADS were as follows: reduction of nucleus, chromatin condensation and nuclear membrane rupture. The flow cytometry with PI straining showed that after 24 hours of DADS treatment the apoptosis rate of K562 cells increased from 11.60 ± 0.83% at the concentration of 10 mg/L to 37.94 ± 0.87% at the concentration of 40 mg/L. The apoptosis rate of K562 cells increased from 37.94 ± 0.87% (24 hours) to 47.02 ± 0.66% (72 hours) after treatment with DADS of 10 mg/L increasing to 40 mg/L DADS. The Fas mRNA expression levels of the related apoptotic genes increased after K562 cells were treated with different concentrations of DADS for 48 hours, while FasL mRNA expression decreased significantly after DADS treatment for 48 hours, compared with those in the control group (p < 0.05). It is concluded that DADS can induce the apoptosis of human leukemia K562 cells in a time-and concentration-dependent manners. The activation of Fas/FasL pathway may play an important role in the K562 cell apoptosis induced by DADS, which is associated with increasing Fas gene expression and decreasing FasL gene expression.
authors: Department of Pediatrics, The First Affilliated Hospital of Nanhua University, Hengyang 421001, Hunan Province, China. xcyin108@sina.com
authors: Xiao-Cheng
authors: XC
authors: Yin
authors: Yan-Hui
authors: YH
authors: Peng
authors: Zheng-Xiang
authors: ZX
authors: Xiao
mesh_terms: D000498:Allyl Compounds / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D004220:Disulfides / Q000494:pharmacology*; D053222:Fas Ligand Protein / Q000378:metabolism*; D015973:Gene Expression Regulation, Leukemic; D006801:Humans; D020014:K562 Cells; D015398:Signal Transduction; D019014:fas Receptor / Q000378:metabolism*
chemical_list: D000498:Allyl Compounds; D004220:Disulfides; C491901:FAS protein, human; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D019014:fas Receptor; C028009:diallyl disulfide