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肿瘤坏死因子相关凋亡诱导配体诱导的细胞凋亡在再生障碍性贫血发病中的意义 被引量:3

The significance of TRAIL-induced apoptosis in aplastic anemia
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摘要 目的通过检测肿瘤坏死因子相关凋亡诱导配体(TRAIL)诱导正常骨髓单个核细胞(BMMNC)凋亡率,及抑制TRAIL凋亡途径后再生障碍性贫血(AA)患者骨髓单个核细胞凋亡率,探讨TRAIL在AA患者骨髓造血细胞凋亡中的作用。方法采用流式细胞术检测43例骨髓象正常者(正常组)及TRAIL作用后(TRAIL组)其骨髓单个核细胞凋亡率;14例AA患者(AA组)及TRAIL抗体作用后(TRAIL-Ab组)其骨髓单个核细胞凋亡率。结果 (1)AA组凋亡率较正常组明显增高,差异有统计学意义(P<0.05)。(2)TRAIL组(浓度为30 ng/ml,作用24 h)凋亡率[(39.98±4.594)%]高于正常组[(19.90±6.656)%],差异有统计学意义(P<0.05)。(3)TRAIL-Ab组凋亡率[(30.28±4.594)%]较AA组[(51.29±7.355)%]减少,差异有统计学意义(P<0.05)。结论一定浓度的TRAIL可使正常骨髓单个核细胞凋亡增加,抑制TRAIL诱导的凋亡途径后,AA患者骨髓单个核细胞凋亡减少,提示TRAIL诱导的细胞凋亡,可能在AA发病中发挥一定作用。 Objective To explore the role of tumor necrosis factor related apoptosis inducing ligand (TRAIL) on aplastic anemia bone marrow mononuclear cell(BMMNC), and approach its effect on the apoptosis of haemopoietic stem cell. By detecting TRAIL induction of normal BMMNC apoptosis rate, and the aplastic anemia BMMNC apoptosis rate after blocking the TRAIL apoptotic pathway. Methods We use flow cytometry to detect the BMMNC apoptosis rate including 43 cases (normal group) and after TRAIL effecting (TRAIL group); 14 cases with aplastic anemia (AA group) and after TRAIL antibody effecting (TRAIL-Ab group). Results (1)Aplastic anemia apoptosis rate was higher than normal group. (2)The apoptosis rate (39.98±4.594)%of TRAIL group(concentration of 30 ng/ml, 24 h) was higher than the normal group (19.90±6.656)%(P〈0.05). (3)The apoptosis rate of TRAIL-Ab group (30.28±4.594)%was lower than aplastic anemia group (51.29±7.355)%(P〈0.05). Conclusions The TRAIL of a certain concentration can make normal BMMNC apoptosis increases, if block the apoptotic pathway induced by TRAIL, the BMMNC apoptosis of aplastic anemia patients will decrease, suggesting that the cell apoptosis induced by TRAIL may play a role in the onset of aplastic anemia.
出处 《中华临床医师杂志(电子版)》 CAS 2014年第5期13-16,共4页 Chinese Journal of Clinicians(Electronic Edition)
基金 山西省太原市科技项目(11027608)
关键词 受体 肿瘤坏死因子 贫血 再生障碍性 细胞凋亡 骨髓单个核细胞 Receptors,tumor necrosis factor Anemia,aplastic Apoptosis Bone marrow mononuclear cell
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参考文献17

  • 1Zheng M, Zheng K, Zllou J, et al. Tcf-1 gene silence suppresses downstream gene expression in CD4+ T cell from bone marrow of aplastic anemia patients[J]. Ann Hematol, 2012, 91(3): 353-358.
  • 2邵宗鸿,袁烨.再生障碍性贫血免疫发病机制及免疫治疗[J].中国实用内科杂志:临床前沿版,2006,26(2):252-255. 被引量:83
  • 3Omokaro SO, Desierto MJ, Eckhaus MA, et al. Lympbocytes with aberrant expression of Fas or Fas ligand attenuate immune bone marrow failure in a mouse model[J]. J Immunol, 2009, 182(6): 3414-3422.
  • 4傅爱林,伍世礼,玄风华.再生障碍性贫血造血细胞Fas抗原表达与T淋巴细胞功能的研究[J].江西医学院学报,2004,44(1):10-13. 被引量:3
  • 5Fischer U, Ruckert C, Hubner B, et al. CD34+ gene expression profiling of individual children with very severe aplastic anemia indicate a pathogenic role of integrin receptors and the proapoptotic death ligand TRAIL[. Haematologica, 2012, 97(9): 1304-1311.
  • 6陆再英,钟南山.内科学.7版[M].北京:人民卫生出版社,2008:381-386.
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  • 8Plpott NJ, Scopes J, Marsh JC, et al. Increased apoptosis in aplastic anemia bone marrow progenitor cell: possible pathophysiologic significan[J]. ExpHematol, 1995, 23(14): 1642-1648.
  • 9Vibhuti, Tripathy NK, Nityanand S. Massive apoptosis of bone marrow cell in aplastic anaemia[J] Bt J Haematoi,2002, 117(4): 993-994.
  • 10Wiley SR, Schooley K, Smolak PJ, otal. Identification and characterization of a new member of the TNF family that induces os[jJ. 1995, 3(6): 673-682.

二级参考文献23

  • 1邵宗鸿,袁烨.再生障碍性贫血免疫发病机制及免疫治疗[J].中国实用内科杂志:临床前沿版,2006,26(2):252-255. 被引量:83
  • 2沈志祥主编.血液科新近展[M].北京:人民卫生出版社,2000.333-351.
  • 3陆再英,钟南山.内科学.7版[M].北京:人民卫生出版社,2008:381-386.
  • 4Zheng M, Zheng K, Zllou J, et al. Tcf-1 gene silence suppresses downstream gene expression in CD4+ T cell from bone marrow of aplastic anemia patients[J]. Ann Hematol, 2012, 91(3): 353-358.
  • 5Omokaro SO, Desierto MJ, Eckhaus MA, et al. Lympbocytes with aberrant expression of Fas or Fas ligand attenuate immune bone marrow failure in a mouse model[J]. J Immunol, 2009, 182(6): 3414-3422.
  • 6Fischer U, Ruckert C, Hubner B, et al. CD34+ gene expression profiling of individual children with very severe aplastic anemia indicate a pathogenic role of integrin receptors and the proapoptotic death ligand TRAIL[. Haematologica, 2012, 97(9): 1304-1311.
  • 7张之南,沈悌.血液病诊断及疗效标准.3版[M].北京:科学出版社:2008:19-23.
  • 8Plpott NJ, Scopes J, Marsh JC, et al. Increased apoptosis in aplastic anemia bone marrow progenitor cell: possible pathophysiologic significan[J]. ExpHematol, 1995, 23(14): 1642-1648.
  • 9Vibhuti, Tripathy NK, Nityanand S. Massive apoptosis of bone marrow cell in aplastic anaemia[J] Bt J Haematoi,2002, 117(4): 993-994.
  • 10Wiley SR, Schooley K, Smolak PJ, otal. Identification and characterization of a new member of the TNF family that induces os[jJ. 1995, 3(6): 673-682.

共引文献103

同被引文献32

  • 1邵宗鸿,袁烨.再生障碍性贫血免疫发病机制及免疫治疗[J].中国实用内科杂志:临床前沿版,2006,26(2):252-255. 被引量:83
  • 2袁烨,邵宗鸿.获得性再生障碍性贫血发病机制的研究进展[J].国际输血及血液学杂志,2006,29(3):200-203. 被引量:9
  • 3陆再英,钟南山.内科学.7版[M].北京:人民卫生出版社,2008:381-386.
  • 4Zheng M, Zheng K, Zllou J, et al. Tcf-1 gene silence suppresses downstream gene expression in CD4+ T cell from bone marrow of aplastic anemia patients[J]. Ann Hematol, 2012, 91(3): 353-358.
  • 5Omokaro SO, Desierto MJ, Eckhaus MA, et al. Lympbocytes with aberrant expression of Fas or Fas ligand attenuate immune bone marrow failure in a mouse model[J]. J Immunol, 2009, 182(6): 3414-3422.
  • 6Fischer U, Ruckert C, Hubner B, et al. CD34+ gene expression profiling of individual children with very severe aplastic anemia indicate a pathogenic role of integrin receptors and the proapoptotic death ligand TRAIL[. Haematologica, 2012, 97(9): 1304-1311.
  • 7张之南,沈悌.血液病诊断及疗效标准.3版[M].北京:科学出版社:2008:19-23.
  • 8Plpott NJ, Scopes J, Marsh JC, et al. Increased apoptosis in aplastic anemia bone marrow progenitor cell: possible pathophysiologic significan[J]. ExpHematol, 1995, 23(14): 1642-1648.
  • 9Vibhuti, Tripathy NK, Nityanand S. Massive apoptosis of bone marrow cell in aplastic anaemia[J] Bt J Haematoi,2002, 117(4): 993-994.
  • 10Wiley SR, Schooley K, Smolak PJ, otal. Identification and characterization of a new member of the TNF family that induces os[jJ. 1995, 3(6): 673-682.

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