【摘 要】
：
目的探讨丙戊酸钠(VPA)诱导K562细胞凋亡的可能机制。方法将K562细胞分为经VPA 2.0 mmol/L处理的实验组(A组)和正常对照组(B组),分别培养24、487、2 h。流式细胞术检测细胞凋
【机 构】
：
扬州大学附属泰兴医院血液病科,南通大学附属医院血液病科,
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目的探讨丙戊酸钠(VPA)诱导K562细胞凋亡的可能机制。方法将K562细胞分为经VPA 2.0 mmol/L处理的实验组(A组)和正常对照组(B组),分别培养24、487、2 h。流式细胞术检测细胞凋亡率和线粒体膜电位改变,分光光度法检测半胱氨酸天门冬氨酸蛋白酶(Caspase)8、Caspase-9蛋白活性。结果 A组细胞凋亡率、细胞线粒体跨膜电位破坏率呈时间依赖性地增加,且明显高于B组(P<0.05);与B组相比,A组不同时间的Caspase-8、Caspase-9活性均上调(P<0.05)。结论 VPA诱导K562细胞凋亡的机制可能与线粒体跨膜电位崩溃或死亡途径有关。
Objective To investigate the possible mechanism of VPA-induced K562 cell apoptosis. Methods K562 cells were divided into experiment group (group A) and control group (group B) treated with 2.0 mmol / L VPA for 24,487 and 2 h respectively. Flow cytometry was used to detect the changes of apoptosis rate and mitochondrial membrane potential, and the activity of caspase-8 and Caspase-9 were detected by spectrophotometry. Results The apoptotic rate of A group and the destruction rate of mitochondrial transmembrane potential increased in a time-dependent manner, and were significantly higher than those in group B (P <0.05). Compared with group B, Caspase-8 and Caspase -9 activity were increased (P <0.05). Conclusion The mechanism of VPA-induced apoptosis in K562 cells may be related to the collapse or death of mitochondrial transmembrane potential.
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