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目的:探讨CAG治疗方案药物阿糖胞苷(Ara-c)、阿克拉霉素(ACR)及粒细胞集落刺激因子(G-CSF)对人T细胞性急性淋巴细胞白血病细胞(Jurkat细胞)的生长抑制和诱导凋亡的情况。方法:用CAG治疗方案药物分别处理Jurkat细胞和缺铁性贫血患者骨髓淋巴细胞,CCK-8法检测细胞增殖抑制率,流式细胞仪检测细胞凋亡率。结果:CAG治疗方案药物作用Jurkat细胞48 h后增殖抑制率为93.67%,与Jurkat细胞PBS对照组比较,差异具有统计学意义(P<0.05);与缺铁性贫血患者骨髓淋巴细胞CAG组比较,差异具有统计学意义(P<0.05)。CAG治疗方案药物作用缺铁性贫血患者骨髓淋巴细胞48 h后增殖抑制率为7.16%,与缺铁性贫血患者骨髓淋巴细胞PBS对照组比较,差异不具有统计学意义(P>0.05)。CAG治疗方案作用Jurkat细胞株12 h后,细胞早期凋亡率为46.12%,晚期凋亡率为5.79%;作用24 h后,细胞早期凋亡率为55.21%,晚期凋亡率为28.31%,Jurkat细胞PBS对照组细胞凋亡率为0,差异具有统计学意义(P<0.05)。结论:CAG治疗方案对缺铁性贫血患者骨髓淋巴细胞的增殖抑制不明显,对缺铁性贫血患者骨髓淋巴细胞副作用小。CAG治疗方案药物能明显抑制Jurkat细胞的生长并杀伤Jurkat细胞,且能诱导较多细胞发生早期、晚期凋亡,凋亡在Jurkat细胞株死亡中起决定性作用,通过凋亡清除绝大多数细胞。
Objective: To investigate the effects of CAG treatment with Ara-c, aclacinomycin (ACR) and granulocyte colony stimulating factor (G-CSF) on human T cell acute lymphoblastic leukemia cells (Jurkat cells) Growth inhibition and induction of apoptosis. Methods: Bone marrow lymphocytes from Jurkat cells and patients with iron deficiency anemia were treated with CAG treatment. The cell proliferation inhibition rate was measured by CCK-8 assay and the apoptosis rate was detected by flow cytometry. Results: The inhibition rate of Jurkat cells treated with CAG for 48 h was 93.67%, which was significantly different from that of Jurkat cells in PBS control group (P <0.05). Compared with CAG group of bone marrow lymphocytes in patients with iron deficiency anemia , The difference was statistically significant (P <0.05). The inhibitory effect of CAG treatment on the proliferation of bone marrow lymphocytes in patients with iron deficiency anemia after 48 h was 7.16%, which was not significantly different from that of PBS control in patients with iron deficiency anemia (P> 0.05). After treated with CAG for 12 h, the early apoptosis rate of Jurkat cells was 46.12% and the late apoptosis rate was 5.79%. The early apoptosis rate was 55.21% and the late apoptosis rate was 28.31% Jurkat cells PBS control group apoptosis rate was 0, the difference was statistically significant (P <0.05). CONCLUSION: CAG treatment has no obvious inhibitory effect on bone marrow lymphocyte proliferation in patients with iron deficiency anemia, and has little side effects on bone marrow lymphocytes in patients with iron deficiency anemia. CAG treatment drugs can significantly inhibit the growth of Jurkat cells and kill Jurkat cells, and can induce more cells in early and late apoptosis, apoptosis plays a decisive role in the death of Jurkat cell lines, most of the cells by apoptosis.