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目的 :研究氧化砷 (As2 O3 )对 K5 6 2细胞增殖和凋亡的作用及其机制。方法 :以细胞形态、细胞生长及活力测定 ,流式细胞仪分析细胞周期相关 DNA含量并以基因组 DNA电泳等方法观察 As2 O3 对 K5 6 2细胞的作用 ,采用 Western印迹和 Northern印迹法就其作用机制进行初步探索。结果 :在 As2 O3 作用下 K5 6 2细胞生长受抑伴随活力下降 ;基因组 DNA电泳出现“梯”状条带 ,流式细胞仪检测出“凋亡峰”。实验进一步表明 As2 O3 可降低该细胞 bcr/abl融合蛋白的含量 ,但不影响 CML 特异性 bcr/abl融合基因的 m RNA水平。结论 :As2 O3 有抑制 K5 6 2细胞增殖和诱导该细胞凋亡的作用。初步研究结果表明 ,As2 O3 导致 bcr/abl融合蛋白含量降低 ,可能参与了作用机制
Objective: To investigate the effect of arsenic trioxide (As2 O3) on the proliferation and apoptosis of K562 cells and its mechanism. Methods: The cell cycle-related DNA content was analyzed by flow cytometry and the effect of As2 O3 on K5 6 2 cells by means of genomic DNA electrophoresis. The effects of As2 O3 on K5 6 2 cells were analyzed by Western blotting and Northern blotting Mechanism to conduct a preliminary exploration. Results: Inhibition of growth of K5 6 2 cells with As 2 O 3 inhibited the viability. The “ladder” bands appeared in genomic DNA electrophoresis and the “apoptosis peak” was detected by flow cytometry. The experiment further shows that As2 O3 can reduce the bcr / abl fusion protein content of the cell, but does not affect the m RNA level of the CML-specific bcr / abl fusion gene. Conclusion: As2 O3 can inhibit the proliferation and induce the apoptosis of K562 cells. Preliminary results show that As2 O3 lead to bcr / abl fusion protein content may be involved in the mechanism of action