Agmatine effects on mitochondrial membrane potential and NF-κB activation protect against rotenone-induced cell damage in human neuronal-like SH-SY5Y cells.

摘要: Agmatine, an endogenous arginine metabolite, has been proposed as a novel neuromodulator that plays protective roles in the CNS several models of cellular damage. However, mechanisms involved these effects neurodegenerative diseases are poorly understood. The present study was undertaken to investigate agmatine on cell injury induced by rotenone, commonly used establishing vivo and vitro Parkinson's disease, human-derived dopaminergic neuroblastoma line (SH-SY5Y). We report dose-dependently suppressed rotenone-induced through reduction oxidative stress. Similar were obtained spermine, suggesting scavenging effect for compounds. unlike also prevented nuclear factor-κB translocation mitochondrial membrane potential dissipation. Furthermore, increase apoptotic markers, such caspase 3 activity, Bax expression cytochrome c release, significantly attenuated with treatment. These findings demonstrate preservation rotenone model death, neuroprotective action appears because suppressing signalling mechanisms. Thus, may have therapeutic treatment disease protecting neurons.