Cepharanthine (CEP) is a bisbenzylisoquinoline alkaloid. Molecular dynamics studies show that CEP interacts with Voltage-dependent anion channel (VDAC), inducing the voltage-independent channel narrowing. In the new conformation, transport between mitochondria and cytoplasm is altered, which leads to the dose-dependent cytotoxicity.

The biological effects of the interaction were investigated on glioblastoma multiforme (SNB-19) and neuronal (PC-12 + NGF) cell lines. The cytotoxic potential of cepharanthine was determined by MTT assay and flow cytometry apoptosis/necrosis studies. T-type calcium channel and VDAC were labelled by the immunocytochemical method. Additionally, fluorescent labelling of reactive oxygen species and mitochondria was performed. Changes in the pore size of VDAC were calculated as well. Molecular dynamics simulations were carried out to examine the interactions of cepharanthine with VDAC.

The obtained results prove that cepharanthine enhances the apoptosis in glioma and neuronal cells by the release of reactive oxygen species. Cepharanthine alters the mitochondria-to-cytoplasm transport and thus induces the cytotoxicity with no selectivity.

头孢兰定（CEP）是一种双苄基异喹啉生物碱。分子动力学研究表明，CEP与电压依赖性阴离子通道（VDAC）相互作用，导致电压依赖性通道变窄。在新的构象中，线粒体和细胞质之间的运输被改变，这导致剂量依赖性细胞毒性。

相互作用的生物学效应研究了胶质母细胞瘤（SNB-19）和神经元（PC-12 + NGF）细胞系。通过MTT测定和流式细胞术凋亡/坏死研究确定头孢兰氨酸的细胞毒性潜力。用免疫细胞化学方法标记T型钙通道和VDAC。另外，对活性氧和线粒体进行荧光标记。还计算了VDAC的孔径变化。进行了分子动力学模拟，以研究头孢兰氨酸与VDAC的相互作用。

所获得的结果证明头孢兰氨酸通过释放活性氧来增强神经胶质瘤和神经元细胞的凋亡。头孢兰氨酸改变了线粒体到细胞质的转运，因此没有选择性地诱导细胞毒性。