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目的 :研究 F as/Fasl系统及凋亡与骨髓增生异常综合征 ( myelodysplastic syndrome,MDS)发生发展的关系。方法 :分别用 TU NEL方法和免疫组化标记方法检测凋亡细胞和 Fas、Fasl表达细胞。而后在光镜下计数相应的阳性细胞并计算其百分率。另外 ,还以 EL ISA方法检测患者血清中的 s Fas的含量。结果 :( 1) MDS组BMMNC中的凋亡细胞百分率 [( 2 2 .83± 10 .14 ) % ]高于正常对照组 [( 2 .2 7± 0 .74) % ] ( P<0 .0 5 ) ;( 2 ) MDS组BMMNC中的 F as表达细胞百分率 [( 2 4.37± 6 .42 ) % ]高于正常对照组 [( 1.93± 0 .32 ) % ] ( P<0 .0 5 ) ;( 3) MDS组BMMNC中的 Fasl表达细胞百分率 [( 2 2 .2 7± 10 .5 0 ) % ]高于正常对照组 [( 4 .18± 1.0 2 ) % ] ( P<0 .0 5 ) ;( 4 ) MDS组血清 s Fas的含量 [( 9.2 4± 10 .5 0 ) μg/L]高于正常对照组 [( 7.5 5± 0 .79) μg/L] ( P<0 .0 5 ) ;( 5 ) MDS组凋亡细胞百分率与 Fas+细胞或 Fasl+细胞百分率之间无直线相关关系 ( P>0 .0 5 )。结论 :实验结果表明 Fas/Fasl系统介导的凋亡以及机体对其调控的失常参与了 MDS骨髓无效造血的病理生理过程。但体内可能还存在另外的机制可引起MDS患者 BMMNC凋亡增加
Objective : To study the relationship between F as/Fasl system and apoptosis and the development of myelodysplastic syndrome (MDS). METHODS: Apoptotic cells and Fas and Fasl-expressing cells were detected by TU NEL and immunohistochemistry, respectively. Then the corresponding positive cells were counted under the light microscope and the percentage was calculated. In addition, the serum s Fas levels were also measured by the EL ISA method. Results: (1) The percentage of apoptotic cells in the BMMNC of the MDS group was higher than that of the normal control group [(2 2. 83 ± 10.14) %] [( 2.27 ± 0.74) %] (P <0. 0 5) (2) The percentage of F as expressing cells in BMMNC in MDS group was higher than that in normal control group [( 2.37 ± 0.64) %] (P <0.05). (3) The percentage of Fasl-expressing cells in BMMNC in the MDS group was higher than that in the normal control group [(2 2.27 ± 10.2) %] (P < .0). 0 5) (4) The serum Fas content in the MDS group was higher than that in the normal control group [( 9.2 4 ± 10 .50) μg/L] [(7.5 5 ± 0 .79) μg/L] (P<0 0.55) (5) There was no linear correlation between the percentage of apoptotic cells in the MDS group and the percentage of Fas+ cells or Fasl+ cells (P> 0.05). Conclusion : The experimental results show that Fas/Fasl system-mediated apoptosis and abnormal regulation of the body participate in the pathophysiological process of MDS bone marrow hematopoiesis. However, there may be additional mechanisms in the body that may cause increased BMMNC apoptosis in MDS patients.