中华眼镜蛇毒组分CⅡ对多药耐药肿瘤细胞的抑制作用  

Inhibition of multidrug-resistant tumor cells induced by fraction CⅡ from naja naja atra venom

作　　者：左长清[1] 林振桃[2] 孔天翰[2] 吴铁[1] 

机构地区：[1]广东医学院药理学教研室 [2]广州医学院蛇毒研究所

出　　处：《中国临床药理学与治疗学》2006年第5期554-557,共4页Chinese Journal of Clinical Pharmacology and Therapeutics

基　　金：广东医学院青年基金资助(№2004218)

摘　　要：目的:研究中华眼镜蛇毒组分CⅡ(FCⅡNNAV)对多药耐药KBv200和K562/A02细胞的抑制作用。方法:应用MTT法观察FCⅡNNAV对KB、KBv200、K562和K562/A02细胞的毒性作用,DNALadder和流式细胞仪观察FCⅡNNAV体外诱导K562/A02凋亡的作用。结果:FCⅡNNAV对KB和耐药KBv200细胞以及K562和耐药K562/A02细胞均有抑制作用,IC50分别为0.87±0.15和1.07±0.08、0.67±0.11和0.75±0.01μg·ml-1。DNALadder和流式细胞仪检测FCⅡNNAV能明显诱导细胞K562/A02凋亡。结论:FCⅡNNAV对敏感细胞KB、K562及耐药细胞KBv200、K562/A02均有较强的抑制作用,FCⅡNNAV能明显诱导耐药K562/A02细胞凋亡,这可能是其抗肿瘤多药耐药机制之一。AIM： To investigate the inhibition of fraction C Ⅱ from naja naja actra venom （FC Ⅱ NNAV） on muhidrug-resistant tumor cell lines KBv200 and K562/ A02. METHODS： Cytotoxicities of FC Ⅱ NNAV on KB, KBv200, K562 and K562/A02 ceils were measured by MTT assay. And the apoptosis induced by FC Ⅱ NNAV on K562/A02 ceils were observed by DNA Ladder and flow cytometry （FCM）. RESULTS： FC ⅡNNAV had the inhibitory effects on KB, KBv200, K562 and K562/A02 cells. The IC50 were 0.87 ± 0.15,1.07 ± 0.08,0.67 ±0.11 and 0.75 ± 0.01 μg· ml^- 1, respectively. It was obvious that FCⅡ NNAV could induce cell apoptosis of K562/A02. CONCLUSION： FC ⅡNNAV has the inhibitory effect on KB, KBv200, K562 and K562/A02 cells. FC ⅡNNAV can induce apoptosis on muhidrug-resistant tumor cell , which may be one of mechanisms for circumventing tumor multidrug-resistant.

关 键 词：蛇毒 肿瘤 多药耐药 凋亡 

分 类 号：R965.2[医药卫生—药理学] R730.5[医药卫生—药学]