Celastrol prevents cadmium-induced neuronal cell death by blocking reactive oxygen species-mediated mammalian target of rapamycin pathway.

ABSTRACT:

Background and purpose

Increasing evidence has suggested cadmium (Cd), as an inducer of ROS, is a potential pathogenic factor in human neurodegenerative diseases. Thus, it is important to find effective interventions for Cd-induced oxidative stress in the CNS. Here, we have studied the effects of celastrol, a plant-derived triterpene, on ROS production and cell death in neuronal cells, induced by Cd.

Experimental approach

PC12, SH-SY5Y cells and primary murine neurons were used to study celastrol neuroprotection against Cd-poisoning. Cd-induced changes in cell viability, apoptosis, ROS and AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway in the cells were analysed by Trypan blue exclusion, DAPI and TUNEL staining, ROS imaging, immunofluorescen

SUBMITTER: Zhang R 

PROVIDER: S-EPMC5341486 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature