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K562/A02的抑制作用及机制。方法:应用MTT法观察FCⅡNNAV体外对K562和K562/A02的毒性作用,流式细胞仪法观察FCⅡNNAV体外对K562/A02细胞Pgp,Bcl2蛋白表达的影响,比色法检测Caspase3活性变化。结果:FCⅡNNAV对耐药K562/A02及敏感K562细胞均有抑制作用,IC50分别为0.75±0.01μg·ml-1和0.67±0.11μg·ml-1。流式细胞仪检测发现FCⅡNNAV能使K562/A02细胞的Pgp,Bcl2蛋白表达明显下调;Caspase3活性明显增强。结论:FCⅡNNAV对细胞K562/A02及细胞K562均有较强的抑制作用,且抑制作用与剂量呈正相关,FCⅡNNAV可能通过抑制K562/A02细胞Pgp,Bcl2蛋白表达,激活Caspase3活性而诱导K562/A02细胞凋亡。
AIM： To investigate the inhibitory effect of fraction C Ⅱ from Naja naja Actra Venom （FC Ⅱ NNAV） on multidrug-resistant human leukemia cell line K562/A02 and its mechanisms. METHODS： The cytotoxicity of FC Ⅱ NNAV on K562/A02 and k562 cells was measured by MTT assay. The protein expression of P-gp and Bcl-2 of K562/A02 was observed by flow cytometry. The activation of Caspase-3 was detected by colorimetric assay. RESULTS： FC Ⅱ NNAV had the inhibitory effect on K562/A02 and K562. The values of IC50 were 0.75±0.01 and 0.67±0.11/μg·ml^-1, respectively. The expression of P-gp and Bcl-2 decreased after application of FC Ⅱ NNAV and Caspase-3 was activated by FC Ⅱ NNAV. CONCLUSION： FC Ⅱ NNAV has the inhibitory effect on K562/A02 and K562. FC Ⅱ NNAV can induce K562/A02 cell apoptosis through down-regulation expression of P-gp and Bcl-2 and activating Caspase-3.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2005年第9期1015-1019,共5页
Chinese Journal of Clinical Pharmacology and Therapeutics
关键词
蛇毒
肿瘤
多药耐药
凋亡
P-糖蛋白
snake venom
neoplasm
multidrug resistance
apoptosis
P-glycoprotein
