Department of Neurosurgery, Qingzhou People's Hospital, Weifang, 262500, China.Department of Neurology, The First People's Hospital of Xianyang, Xianyang, 712000, China.Department of Neurosurgery, Qingzhou Hospital Affiliated to Shandong First Medical University, Weifang, Shandong, 262500, China.AffiliationsDepartment of Neurology, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, 471009, China.
Extensive studies have reported that interaction of α-synuclein amyloid species with neurons is a crucial mechanistic characteristic of Parkinson's disease and small molecules can downregulate the neurotoxic effects induced by protein aggregation. However, the exact mechanism of these neuroprotective effects by small molecules remain widely unknown. In the present study, α-synuclein samples in the amyloidogenic condition were aged for 120 h with or without different concentrations of mitoquinon...更多
Extensive studies have reported that interaction of α-synuclein amyloid species with neurons is a crucial mechanistic characteristic of Parkinson's disease and small molecules can downregulate the neurotoxic effects induced by protein aggregation. However, the exact mechanism of these neuroprotective effects by small molecules remain widely unknown. In the present study, α-synuclein samples in the amyloidogenic condition were aged for 120 h with or without different concentrations of mitoquinone as a quinone derivative compound and the amyloid characteristics and the relevant neurotoxicity were evaluated by Thioflavin T /Nile red fluorescence, Congo red absorption, circular dichroism , transmission electron microscopy , cell viability, lactate dehydrogenase , reactive oxygen species , reactive nitrogen species , malondialdehyde , superoxide dismutase , and caspase-9/-3 activity assays. Results clearly showed the capacity of MitoQ on the inhibition of the formation of α-synuclein fibrillation products through modulation of the aggregation pathway by an effect on the kinetic parameters. Also, it was shown that α-synuclein samples aged for 120 h with MitoQ trigger less neurotoxic effects against SH-SY5Y cells than α-synuclein amyloid alone. Indeed, co-incubation of α-synuclein with MitoQ reduced the membrane leakage, oxidative and nitro-oxidative stress, modifications of macromolecules, and apoptosis.收起
发文期刊《Inhibitory effect of mitoquinone against the α-synuclein fibrillation and relevant neurotoxicity: possible role in inhibition of Parkinson's disease》历年引证文献趋势图
