Graduate School of East-West Medical Science, Kyung Hee University, Gyeoggi-do 446-701, Korea.
Biol Pharm Bull. 2012;35(7):1069-75. doi: 10.1248/bpb.b12-00009.
Autophagy is associated with cell survival and cell death. Autophagy is implicated in the pathophysiology of various human diseases. In order to identify autophagy regulatory molecules, we screened a chemical drug library in SH-SY5Y cells and selected Sertindole as a potent autophagy inducer. Sertindole was developed as an antipsychotic drug for Schizophrenia. Sertindole treatment highly induced the formation of autophagosomes as well as LC3 conversion. Subsequently, Sertindole-induced autophagy was efficiently suppressed by down regulation of ATG5. Sertindole also increased reactive oxygen species (ROS) production, which contributes to autophagy-associated cell death in neuroblastoma cells. ROS scavengers such as N-acetylcysteine and Trolox suppressed not only ROS generation but also autophagy activation by Sertindole. These results suggest Sertindole induces autophagy and autophagy-associated cell death by ROS production in neuroblastoma cells.
自噬与细胞存活和细胞死亡有关。自噬参与了各种人类疾病的病理生理学过程。为了鉴定自噬调节分子,我们在 SH-SY5Y 细胞中筛选了一个化学药物文库,并选择了塞替啶作为一种有效的自噬诱导剂。塞替啶最初被开发为治疗精神分裂症的抗精神病药物。塞替啶处理可高度诱导自噬体的形成以及 LC3 转化。随后,通过下调 ATG5,可有效抑制塞替啶诱导的自噬。塞替啶还增加了活性氧(ROS)的产生,这有助于神经母细胞瘤细胞中与自噬相关的细胞死亡。ROS 清除剂,如 N-乙酰半胱氨酸和 Trolox,不仅抑制了 ROS 的产生,还抑制了塞替啶诱导的自噬激活。这些结果表明,塞替啶通过在神经母细胞瘤细胞中产生 ROS 诱导自噬和自噬相关的细胞死亡。