摘要
目的:观察环抱菌素A对人白血病HL-60细胞株凋亡的影响及其作用机制。方法:采用瑞氏染色、流式细胞仪、TUNEL法观察环孢菌素A对HL-60细胞株凋亡的影响;采用流式细胞仪检测环孢菌素A影响HL-60细胞凋亡时bcl-2基因表达的改变情况。结果:20mg/L环孢菌素A作用6h可诱导HL-60细胞凋亡,瑞氏染色呈现典型的凋亡形态学改变,流式细胞仪显示凋亡峰。细胞周期分析发现,环孢菌素A可使HL-60细胞生长阻滞于G_0-G_1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HL-60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 HL-60 cells and its mechanism. Methods: Apoptosis of HL-60 cells induced by CsA was studied by light microscopy, TdT-mediated dUTP nick end labeling (TUNEL) and flow cytometry (FCM); The effect of CsA on the expresion of bcl-2 gene was detected by FCM. Results: HL-60 cells which were induced by the concentration of 20 mg/L CsA cultured for 6 hours, exhibited typical apoptotic morphological changes under light microscopy. The apoptotic peak was clearly displayed by FCM and HL-60 cells were arrested by CsA in the stage Go to Gi. The apoptosis rate was significandy higher in CsA-treated groups than that in the alcohol group (P < 0. 01) . The expression rate of transcription protein from bcl-2 was significantly lower in CsA-treated groups than that in the alcohol group( P < 0. 01). Conclusion: CsA-induced apoptosis of HL-60 cells is probably associated with down-regulating expression of bcl-2 gene.
出处
《南京医科大学学报（自然科学版）》
CAS
CSCD
北大核心
2003年第6期576-578,共3页
Journal of Nanjing Medical University(Natural Sciences)
