Celastrol promotes apoptotic cell death in children neuroblastoma cells through caspases dependent pathway.

Objective: To investigate the in-depth pharma-cological mechanisms of celastrol in children neuro-blastoma treatment.

Methods: In the current study, we examined the effects of celastrol on children neuroblastoma cells viability and proliferation by cell counting kit-8 assay and colony formation assay. Annexin V-FTIC and PI staining were applied to determine cell apoptosis after celastrol treatment. ROS generation levels were examined by 2', 7'-dichloroflfluorescin diacetate.

Results: We found that celastrol could suppress the proliferation of children neuroblastoma cells with few effects on normal cell lines . Further mechanisms studies have shown that celastrol inhibited cell cycle progression and induced cell apoptosis in QDDQ-NM and SH-SY5Y cells. In addition, ROS production might involve in celastrol-mediated apoptotic cell death in children neuroblastoma cells by activating caspase death pathway.

Conclusions: Our findings demonstrated that celastrol could promote ROS generation-induced apoptosis in neuroblastoma cell by activating caspase death pathway. These findings suggested that celastrol might be a potential novel anti-neuroblastoma agent with minor cytotoxicity.