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非重型再生障碍性贫血患者血清对32D细胞凋亡及Stat3蛋白磷酸化的影响

林赠华 刘红 姜胜华 陆伟 宋国齐 李俊宏

山东医药2011,Vol.51Issue(37):16-18,3.
山东医药2011,Vol.51Issue(37):16-18,3.

非重型再生障碍性贫血患者血清对32D细胞凋亡及Stat3蛋白磷酸化的影响

Effects of sera from patients with non severe aplastic anemia on the apoptosis and expression of phosphorylated Stat3 protein in 32D cells

林赠华 1刘红 1姜胜华 1陆伟 1宋国齐 1李俊宏1

作者信息

  • 1. 南通大学附属医院,江苏南通226001
  • 折叠

摘要

Abstract

Objective To investigate the expression of phosphorylated Stal3 protein in apoptosis of the myeloid progenitor cell line 32 D induced by sera from patients with non severe aplastic anemia (NSAA). Methods The expressions of phosphorylated Stat3 protein in the 32D cells were determined by Western blot after treated with normal sera or sera from patients with NSAA for 0, 12, 24, 36 and 48 hours. After treated with sera for 24 hours, the 32 D cells were subjected to apoptosis analysis using flow cytometry, while cell counting and trypan blue staining were performed to assess cell number and cell viability, respectively. Results The higher expressions of phosphorylated Stat3 protein were found in the NSAA group after treated with sera for 12, 24, 36 and 48 hours and the difference in the two groups was maximal at 24 hours after treated with sera ( P <0.05). At 24 hour point after treated with sera, the NSAA group had more apoptotic cells and lower cell numbers compared with those of the control group (P<0.05) , however, there was no significant difference in cell viability between the two groups. Conclusions 24-hour treatment with sera from patients with NSAA can induce apoptosis of 32 D cells and up-regulate the phosphorylated Stat3 expression in vitro. Phosphorylated Stat3 may be involved in the apoptosis of 32D cells induced by sera from patients with NSAA.

关键词

贫血,再生障碍性/细胞凋亡/信号转导子和转录激活子3

Key words

anemia,aplastic/ apoptosis/ Stat3

分类

医药卫生

引用本文复制引用

林赠华,刘红,姜胜华,陆伟,宋国齐,李俊宏..非重型再生障碍性贫血患者血清对32D细胞凋亡及Stat3蛋白磷酸化的影响[J].山东医药,2011,51(37):16-18,3.

基金项目

国家自然科学基金项目(81070400):江苏省卫生厅兴卫工程医学重点人才基金(RC2007084) (81070400)

南通市科技计划社会发展项目(S2010023). (S2010023)

山东医药

1002-266X

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