中华眼镜蛇毒组分CⅡ诱导多药耐药白血病细胞K562/A02凋亡  

Apoptosis of Multidrug-resistant Human Leukemia Cell Line K562/A02 Induced by Fraction CⅡ from Naja Naja Actra Venom

作　　者：左长清[1] 林振桃[1] 孔天翰[1] 

机构地区：[1]广州医学院蛇毒研究所,广东广州510182

出　　处：《广州医学院学报》2004年第3期26-30,共5页Academic Journal of Guangzhou Medical College

摘　　要：目的 :研究中华眼镜蛇毒组分CⅡ (FCⅡNNAV)对多药耐药白血病细胞K5 6 2 /A0 2的抑制作用及机制。方法 :应用MTT法、荧光显微镜法、流式细胞仪法 ,观察FCⅡNNAV单用及联合阿霉素 (ADM)体外对K5 6 2 /A0 2的毒性作用、凋亡作用及对Bcl 2表达的影响。结果 :FCⅡNNAV单用对耐药K5 6 2 /A0 2及敏感K5 6 2细胞均有抑制作用 ,IC50 分别为 (0 .75± 0 .0 1) μg/mL和 (0 .6 7± 0 .11) μg/mL。FCⅡNNAV联合ADM体外对细胞K5 6 2 /A0 2有较强的协同抑制作用。荧光显微镜、流式细胞仪检测FCⅡNNAV能明显诱导细胞K5 6 2 /A0 2凋亡 ,凋亡率呈剂量依赖性增加。流式细胞仪检测发现FCⅡNNAV能使细胞K5 6 2 /A0 2的Bcl 2表达下调 ,表达率呈剂量依赖性减少。结论 :FCⅡNNAV对细胞K5 6 2 /A0 2及细胞K5 6 2均有较强的抑制作用 ,且抑制作用与剂量呈正相关 ,并与抗癌药ADM有较强协同作用。FCⅡNNAV能明显诱导K5 6 2 /A0 2细胞凋亡 ,其机制可能与Bcl 2表达下调有关。Objective:To investigate the inhibition of Fraction CⅡ from Naja Naja Actra Venom(FCⅡNNAV) on multidrug-resistant human leukemia cell line K562/A02 and its mechanism.Methods:the cytotoxicity of FCⅡNNAV on K562/A02 cell was measured by MTT assay.The apoptosis of FCⅡNNAV on K562/A02 cell was surveyed with fluorescent microscope and flow cytometry(FCM).The protein expression of Bcl-2 of K562/A02 was observed by flow cytometry.Results:FCⅡNNAV had the inhibitory effect on K562/A02 and K562/S.The IC 50 were (0 75±0.01) μg/mL and (0.67±0.11) μg/mL, respectively. Combination of FCⅡNNAV and ADM exhibited synergistic effect on K562/A02 cell.It was obvious that FCⅡNNAV induced K562/A02 cell apoptosis.And the apoptosis rate of K562/A02 cell was obviously dose-dependant on FCⅡNNAV.The protein expression of Bcl-2 was down-regulated.Conclusion:FCⅡNNAV had inhibition effect on K562/A02 and K562/S, and synergistic effect on K562/A02 cell in combination of ADM.FCⅡNNAV could induce apoptosis on K562/A02 cell through down-regulating the expression of Bcl-2.

关 键 词：蛇毒 肿瘤 多药耐药 凋亡 

分 类 号：R7336[医药卫生—肿瘤]