摘要
为了探讨三氧化二砷 (As2 O3)对多发性骨髓瘤 (MM )细胞株KM3的作用及其可能机制 ,用台盼蓝拒染法检测细胞生长抑制率 ,用光镜、透射电镜观察形态变化 ,用DNA电泳观察As2 O3诱导KM3细胞凋亡 ,用流式细胞仪检测细胞周期的变化 ,用TRAP PCR ELISA法检测As2 O3作用KM3细胞后的端粒酶活性变化 ,并用半定量RT PCR法检测端粒酶逆转录酶 (hTERTmRNA)的表达水平。结果表明 :As2 O3抑制KM3细胞的生长 ,具有诱导细胞凋亡的作用 ;As2 O3阻滞细胞于G2 期 ;As2 O3可抑制KM3细胞的端粒酶活性和hTERTmRNA的表达 ,且hTERTmRNA下降趋势与端粒酶活性相一致。结论 :端粒酶及其逆转录酶活性的下调可能在As2 O3诱导KM3细胞凋亡的过程中起了重要作用。
To explore the effects of arsenic trioxide on multiple myeloma (MM) cell line KM 3 and its possible mechanism,cell viability was counted by trypan-blue exclusion,apoptosis was detected by morphology and DNA ladder;cell cycle was assayed by flow cytometry (FCM),telomerase activity was determined by semi-quantitative telomeric repeat amplification protocol (TRAP)-reverse transcription polymerase chain reaction (RT-PCR)-enzyme linked immunosorbent assay (ELISA),while the expression of hTERT mRNA in transcriptional level was measured by using RT-PCR. The results showed that arsenic trioxide inhibited the growth and viability of KM 3 cell and induced apoptosis;cell cycle was arrested in G 2 phase;arsenic trioxide could inhibit telomerase activity,which consisted with the downtrend of hTERT mRNA expression. In conclusion,down-regulation of telomerase activity and hTERT may play an important role in the apoptosis of MM cell line KM 3 induced by arsenic trioxide.
出处
《中国实验血液学杂志》
CAS
CSCD
2004年第3期346-349,共4页
Journal of Experimental Hematology
