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作 者:曾赟[1]
出 处:《南通大学学报(医学版)》2011年第2期101-102,105,共3页Journal of Nantong University(Medical sciences)
基 金:国家自然科学基金资助项目(31070723)
摘 要:目的:观察环孢菌素A对K562细胞株凋亡的影响及其作用机制。方法:采用瑞氏染色、流式细胞术观察环孢菌素A对K562细胞株凋亡的影响;采用流式细胞仪检测环孢菌素A影响K562细胞凋亡时Bcl-2基因表达的改变情况。结果:20μmol/L环孢菌素A作用24 h可诱导K562细胞凋亡,瑞氏染色呈现典型的凋亡形态学改变,流式细胞术显示凋亡峰,细胞周期分析发现环孢菌素A可使K562细胞生长阻滞于G0~G1期。环孢菌素A处理组的凋亡率高于对照组(P〈0.01);环孢菌素A处理组的Bcl-2蛋白阳性率低于对照组(P〈0.01)。结论:环孢菌素A可诱导K562细胞株凋亡,其机制可能是通过下调Bcl-2基因表达。Objective: To investigate the effect of CsA on apoptosis of K562 cells and identify the mechanism of CsA-induced apoptosis in K562 cells.Methods: Apoptosis of K562 cells induced by CsA was studied by light microscopy and flow cytometry(FCM).The effect of CsA on the expression of Bcl-2 gene was detected by FCM.Results: 20 μmol/L CsA induced the apoptosis of K562 cells in culture for 24 hours,on examining with light microscopy apoptotic cells showed typical morphological change of apoptosis,apoptotic cells displayed apoptotic peak when measured by FCM.CsA arrested K562 cells at G0~G1 phase.The apoptosis rate was significantly higher in CsA-treated groups than that in the alcohol group(P0.01).The expression rate of Bcl-2 oncoprotein was significantly lower in CsA-treated groups than that in the alcohol group(P0.01) Conclusion: CsA can induce apoptosis in K562 cells by down-regulating Bcl-2 gene in protein level.
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