[硫特通过激活氧化应激诱导骨髓增生异常综合征细胞凋亡】。]

Qiang-An Jing, Chao-Ting Zhou, Yun-Yi Wu, Xia Ke, Xiang-Min Tong
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引用次数: 0

摘要

目的探讨噻替特是否能抑制骨髓增生异常综合征(MDS)细胞的增殖并诱导其凋亡:方法:采用 CCK-8 法检测噻替特对 MDS 细胞株 SKM-1 的细胞毒性,以及 GSH、NAC 和 Z-VAD-FMK 对噻替特诱导的细胞活力抑制的逆转作用。EdU检测法用于检测细胞的增殖能力。细胞内活性氧(ROS)在 DCFH-DA 染色后通过流式细胞仪进行测定。通过 Western 印迹检测 DNA 损伤和细胞凋亡相关蛋白的表达:结果:硫代硫醇处理明显抑制了 SKM-1 细胞的活力和增殖能力。结果:硫代硫醇处理可明显抑制 SKM-1 细胞的活力和增殖能力,观察到大量 ROS 生成,C-PARP、C-Caspase 3 和 γ-H2AX 明显升高,而 BCL-2 则明显降低。此外,GSH、NAC和Z-VAD-FMK能够减轻硫特对SKM-1细胞的细胞毒性:结论:硫妥泰可通过介导 ROS 生成和促凋亡蛋白表达来促进 MDS 细胞凋亡。
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[Thiotert Induces Myelodysplastic Syndromes Cells Apoptosis by Activating Oxidative Stress].

Objective: To explore whether thiotert treatment can inhibit proliferation and induce apoptosis in myelodysplastic syndromes (MDS) cells.

Methods: CCK-8 assay was used for determining the cytotoxicity of thiotert to MDS cell line SKM-1 and the reversal effect of GSH, NAC, and Z-VAD-FMK on thiotert-induced inhibition of cell viability. EdU assay was deployed to detect the cell proliferation ability. Intracellular reactive oxygen species (ROS) was measured by flow cytometry after DCFH-DA staining. The expression of DNA damage- and apoptosis-related proteins was detected by Western blot.

Results: Thiotert treatment significantly suppressed the cell viability and proliferation ability in SKM-1 cells. A large amount of ROS generation and markedly elevated C-PARP, C-Caspase 3, and γ-H2AX were observed after thiotert administration, while BCL-2 was significantly decreased. In addition, GSH, NAC, and Z-VAD-FMK were able to mitigate the cytotoxicity of thiotert on SKM-1 cells.

Conclusion: Thiotert can promote MDS cell apoptosis by mediating ROS production and pro-apoptotic proteins expression.

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来源期刊
中国实验血液学杂志
中国实验血液学杂志 Medicine-Medicine (all)
CiteScore
0.40
自引率
0.00%
发文量
7331
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