Guanosine exerts neuroprotective effects by reversing mitochondrial dysfunction in a cellular model of Parkinson's disease

摘要: The mitochondria are the most important cytoplasmic organelles in determining cell survival and death. Mitochondrial dysfunction leads to a wide range of disorders, including neurodegenerative diseases. central events mitochondrial‑dependent death pathway activation mitochodrial permeability transition pore (mPTP) disruption mitochondrial membrane potential, which cause release apoptogenic molecules finally lead This is thought be at least partly responsible for loss dopaminergic neurons Parkinson's disease (PD); thus, attenuation may contribute alleviating severity progression this disease. Guanosine pleiotropic molecule affecting multiple cellular processes, growth, differentiation survival. Its protective effects on nervous system several types by inhibiting apoptosis have been shown number pathological conditions. study aimed analyze ability guanosine protect neuronal PC12 cells from toxicity induced 1-methyl-4-phenylpyridinium (MPP+), active metabolite 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), mediates selective damage causes irreversible Parkinson-like symptoms humans primates. Our results demonstrated that MPP+ was significantly prevented pre-treatment 3 h with guanosine. In addition, attenuated MPP+-induced collapse transmembrane potential sebsequent caspase-3, thereby protecting against stress-induced damage.