Impaired homeostasis of
copper has been linked to different pathophysiological mechanisms in
neurodegenerative diseases and oxidative injury has been proposed as the main mechanism. This study aims to use
curcumin, a widely used antioxidative and anti-apoptotic agent, to exert the
neuroprotective effect against
copper in vitro and illuminate the underlying mechanism. The effect of
curcumin was examined by using a cell counting kit-8 assay, flow cytometry, immunofluorescence, spectrophotometer, and western blot. Results revealed that after pretreatment with
curcumin for 3 h,
copper-induced toxicity and apoptosis show a significant decline. Further experiments showed that
curcumin not only decreased the production of ROS and MDA but also increased the activities of the ROS scavenging
enzymes SOD and CAT. Moreover,
curcumin treatment alleviated the decrease in mitochondrial membrane potential and the nuclear translocation of
cytochrome c induced by
copper. The
protein levels of
pro-caspase 3,
pro-caspase 9, and PARP1 were up-regulated and the Bax/Bcl-2 ratio was down-regulated in the presence of
curcumin. Taken together, our study demonstrates that
curcumin has neuroprotective properties against
copper in SH-SY5Y cells and the potential mechanisms might be related to oxidative stress and mitochondrial apoptosis.