Protective Effects of Curcumin on Amyloid-β-Induced Neuronal Oxidative Damage

To investigate the protective effects of curcumin against amyloid-beta (A beta)-induced neuronal damage. Primary rat cortical neurons were cultured with different treatments of A beta and curcumin. Neuronal morphologies, viability and damage were assessed. Neuronal oxidative stress was assessed, including extracellular hydrogen peroxide and intracellular reactive oxygen species. The abilities of curcumin to scavenge free radicals and to inhibit A beta aggregation and beta-sheeted formation are further assessed and discussed. Curcumin preserves cell viability, which is decreased by A beta. The results of changed morphology, released Lactate dehydrogenases and cell viability assays indicate that curcumin protects A beta-induced neuronal damage. Curcumin depresses A beta-induced up-regulation of neuronal oxidative stress. The treatment sequence impacts the protective effect of curcumin on A beta-induced neuronal damage. Curcumin shows a more protective effect on neuronal oxidative damage when curcumin was added into cultured neurons not later than A beta, especially prior to A beta. The abilities of curcumin to scavenge free radicals and to inhibit the formation of beta-sheeted aggregation are both beneficial to depress A beta-induced oxidative damage. Curcumin prevents neurons from A beta-induced oxidative damage, implying the therapeutic usage for the treatment of Alzheimer's disease patients.