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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 investigate the mechanism of cell apoptosis induced by C component of cobra venom from U251 human glioma cell line. Methods The C cobra venom C component was divided into 1.5 mg / L (group A), 3.0 mg / L (group B), 4.5 mg / L (group C) and 15.0 mg / L (D group) and 30.0 mg / L (group E). The positive control group was treated with 40.0 mg / L cisplatin (DDP) and another negative control group. DNA gel electrophoresis The apoptosis of FC was observed. The expression of bcl-2 / bax gene was detected by immunohistochemistry (SP) and reverse transcriptase-polymerase chain reaction (RT-PCR) Results The C cobra venom C induced the apoptosis of U251 cells. The apoptosis rate of U251 cells induced by FC was closely related to the drug concentration (P <0.01). The expression of bcl-2 / bax did not change significantly . Conclusion FC has the effect of inducing apoptosis in U251 cells, but its induction of apoptosis does not depend on the change of bcl-2 / bax gene.