CAJ | 학술논문

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.
목적:탐토CAG치료방안약물아당포감(Ara-c)、아극랍매소(ACR)급립세포집락자격인자(G-CSF)대인T세포성급성림파세포백혈병세포(Jurkat세포)적생장억제화유도조망적정황.방법:용CAG치료방안약물분별처리Jurkat세포화결철성빈혈환자골수림파세포,CCK-8법검측세포증식억제솔, 류식세포의검측세포조망솔. 결과:CAG치료방안약물작용Jurkat세포48 h후증식억제솔위93.67%,여Jurkat세포PBS대조조비교,차이구유통계학의의(P<0.05);여결철성빈혈환자골수림파세포CAG조비교,차이구유통계학의의(P<0.05). CAG치료방안약물작용결철성빈혈환자골수림파세포48 h후증식억제솔위7.16%, 여결철성빈혈환자골수림파세포PBS대조조비교, 차이불구유통계학의의 (P>0.05). CAG치료방안작용Jurkat세포주12 h후,세포조기조망솔위46.12%,만기조망솔위5.79%;작용24 h후,세포조기조망솔위55.21%,만기조망솔위28.31%,Jurkat세포PBS대조조세포조망솔위0,차이구유통계학의의(P<0.05). 결론:CAG치료방안대결철성빈혈환자골수림파세포적증식억제불명현,대결철성빈혈환자골수림파세포부작용소.CAG치료방안약물능명현억제Jurkat세포적생장병살상Jurkat세포,차능유도교다세포발생조기、만기조망,조망재Jurkat세포주사망중기결정성작용,통과조망청제절대다수세포.
Objective: To investigate the inhibition of proliferation and enhancement of apoptosis in Jurkat cells induced by CAG regimen. Methods: Jurkat cells and bone marrow cells of patients with iron deficiency anemia were treated by CAG regimen (G-CSF,Ara-C and ACR), and the proliferation inhibition of the cell was detected by CCK-8 assay. The apoptosis rate was detected by flow cytometry in Annexin V FLUOS Staining Kit. Results: The inhibitory proliferation rate of CAG regimen in the Jurkat cells by 48 h was 93.67%, which was significantly higher than that of PBS control group of Jurkat cells. The inhibitory proliferation rate of CAG regimen in the Jurkat cells by 48 h was 91.92%. Compared with CAG regimen on the patients with iron deficiency anemia,the result is statistically significant (P < 0.05). The inhibitory proliferation rate of CAG regimen in the patients with iron deficiency anemia by 48 h was 7.16%, and the difference was not significant between CAG and PBS in patients with iron deficiency anemia. After 12 h treatmemnt by CAG regimen, the early apoptosis rate of Jurkat cells was 46.12%, and the late apoptosis rate was 5.79%. After 24 h treatment by CAG regimen, the early apoptosis rate of cells was 55.21%, and the late apoptosis rate was 28.31%. After the treatmemnt by PBS, the apoptosis rate of Jurkat cells was 0%. The result is statistically significant (P< 0.05). Conclusion: The inhibition of proliferation in bone marrow cells treated by the CAG regimen was not obvious. CAG regimen can significantly inhibit the proliferation of Jurkat cells and kill Jurkat cells. CAG regimen can also induce early and late apoptosis, which suggest that apoptosis play a decisive role in the death of Jurkat cells, and the majority of cells be cleared by the apoptosis.