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目的 探讨人类端粒酶逆转录酶 (hTERT)基因反义寡核苷酸 (ASODN)对顺铂诱导原代培养的急性髓细胞白血病 (AML M2 )、慢性髓细胞白血病 (CML)细胞凋亡的影响。方法 采用锥虫蓝拒染法观察hTERTASODN与顺铂联合对AML、CML细胞生存的影响。琼脂糖凝胶电泳分析细胞凋亡的DNA断裂 ;通过流式细胞仪对细胞凋亡峰进行定量分析。结果 hTERT基因ASODN作用于AML、CML细胞 2 4h再加入顺铂对AML、CML细胞的生存均具有很明显的抑制作用 ,分别同正义寡核苷酸(SODN)联合顺铂组、单用顺铂组进行比较 ,差异有显著性 (P <0 0 1)。hTERTASODN作用于AML、CML细胞 2 4h再加入顺铂 ,经琼脂糖凝胶电泳即可见到DNA梯形条带 ,并且凋亡细胞百分率( 4 2 68%,3 5 72 %)分别与SODN联合顺铂组 ( 2 9 0 2 %,2 3 84 %)、单用顺铂组 ( 2 7 5 3 %,2 1 0 2 %)进行比较 ,差异有显著性 (P <0 0 1)。结论 hTERT基因反义寡核苷酸可促进顺铂诱导AML、CML细胞凋亡。
Objective To investigate the apoptosis of primary cultured acute myeloid leukemia (AML M2) and chronic myeloid leukemia (CML) cells induced by human telomerase reverse transcriptase (hTERT) antisense oligonucleotide (ASODN). influences. Methods Trypan blue exclusion was used to observe the effects of hTERTASODN and cisplatin on the survival of AML and CML cells. DNA fragmentation of apoptosis was analyzed by agarose gel electrophoresis; the apoptotic peak was quantified by flow cytometry. Results hTERT gene ASODN acted on AML and CML cells for 24 hours and then added cisplatin to inhibit the survival of AML and CML cells. They were combined with sense oligonucleotides (SODN) and cisplatin groups, respectively. There was a significant difference between the groups (P < 0 01). hTERTASODN acted on AML and CML cells for 24 hours and then added cisplatin. DNA ladders could be seen by agarose gel electrophoresis, and the percentage of apoptotic cells (4426.8%, 3472%) were combined with SODN and cisplatin respectively. The differences were statistically significant (P < 0 01) between the groups (2902%, 2344%) and cisplatin alone (275.3%, 2102%). Conclusion hTERT antisense oligonucleotide can promote the apoptosis of AML and CML cells induced by cisplatin.