摘要
目的以人神经胶质瘤细胞系U251为实验对象,研究中华眼镜蛇毒C组分诱导细胞凋亡的的机制。方法将中华眼镜蛇毒C组分分为1．5 mg／L(A组),3．0 mg／L(B组),4．5 mg/L (C组),15．0 mg／L(D组)和30．0 mg／L(E组)5个浓度组,以顺铂(DDP)40．0 mg／L为阳性对照组, 另设一阴性对照组,采用DNA凝胶电泳检测法,观察FC诱导细胞凋亡的情况;采用免疫组织化学法(SP)和逆转录-聚合酶链反应(RT-PCR)法检查bcl-2／bax基因的表达。结果中华眼镜蛇毒C 组分对U251细胞具有诱导凋亡的作用,FC诱导U251细胞凋亡率与药物浓度密切相关(P< 0．01),使用FC前后,bcl-2／bax表达无显著变化。结论 FC有诱导U251细胞凋亡的作用,但其诱导凋亡不依赖于bcl-2／bax基因的改变。
Objective To study the mechanism of apoptosis induced by Fraction C from Naja Naja AtraVenom （FC） in human glioma cell line U251. Methods U251 cells were treated with Aidi that have been prepared with 1.5 mg/L （group A）, 3.0 mg/L （group B）, 4.5 mg/L/ml （group C）, 15.0 mg/L （group D） and DDP （40mg/L, group E） as positive control group. U251 cells nottreated with drugs served as negative control group. The change of U251 cells was observed under the invented microscopy. Apoptosis of U251 cells was detected by DNA ladder. Gene expression related with apoptosis was examined by immunohistochemical method. Results Apoptosis rate induced by FC was concentration-dependent （P 〈0.01）. When the concentration of FC was over 4.5 mg/L, the gene expression of bcl-2/bax had no significant differences as compared with control group. Conclusion FC can induce apoptosis of U251 cell, which is not bcl-2/bax-dependent.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2006年第5期560-562,i0002,共4页
Chinese Journal of Experimental Surgery
基金
深圳市科技局计划课题资助项目(200404063)
