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Proteasome Inhibition Induces Glutathione Synthesis and Protects Cells from Oxidative Stress
TLDR
The data suggest that proteasome inhibition afforded cytoprotection against oxidative stress by the elevation of glutathione content, and its elevation was mediated by p38 MAPK phosphorylation. Expand
Proteasome Mediates Dopaminergic Neuronal Degeneration, and Its Inhibition Causes α-Synuclein Inclusions*
TLDR
The proteasome plays an important role in both inclusion body formation and dopaminergic neuronal death but these processes form opposite sides on the proteasomesome regulation in this model. Expand
Nicotinic receptor stimulation protects nigral dopaminergic neurons in rotenone‐induced Parkinson's disease models
TLDR
The results suggest that the rotenone mouse model may be useful for assessing candidate antiparkinson agents, and that nAChR (nicotinic acetylcholine receptor) stimulation can protect DA neurons against degeneration. Expand
p‐quinone mediates 6‐hydroxydopamine‐induced dopaminergic neuronal death and ferrous iron accelerates the conversion of p‐quinone into melanin extracellularly
TLDR
It is suggested that generation of p‐quinone played a pivotal role in 6‐OHDA‐induced toxicity and extracellular iron in contrast to intracellular iron was protective rather than harmful because it accelerated the conversion of p-quinone into melanin. Expand
Elevation of heme oxygenase‐1 by proteasome inhibition affords dopaminergic neuroprotection
TLDR
The results suggest that mesencephalic HO‐1 protein level is regulated by proteasome activity and the elevation by prote asome inhibition affords neuroprotection. Expand
Novel neuroprotective mechanisms of pramipexole, an anti-Parkinson drug, against endogenous dopamine-mediated excitotoxicity.
TLDR
It is suggested that pramipexole protects dopaminergic neurons from glutamate neurotoxicity by the reduction of intracellular dopamine content, independently of dopamine D2-like receptor activation. Expand
Iron accelerates the conversion of dopamine‐oxidized intermediates into melanin and provides protection in SH‐SY5Y cells
TLDR
It is demonstrated that thiol antioxidants provided almost complete protection from dopamine‐mediated toxicity in SH‐SY5Y, a human neuroblastoma cell line, and addition of iron inhibited dopamine‐induced cytotoxicity, suggesting that iron can provide protection when it accelerates the conversion of dopamine oxidation intermediates. Expand
Vulnerability to glutamate toxicity of dopaminergic neurons is dependent on endogenous dopamine and MAPK activation
TLDR
It is demonstrated that dopaminergic neurons were preferentially affected by glutamate toxicity in rat mesencephalic cultures, and one of the mechanisms may be an enhancement of dopamine synthesis mediated by ERK. Expand
Compensatory role of the Nrf2-ARE pathway against paraquat toxicity: Relevance of 26S proteasome activity.
TLDR
Data indicate that the compensatory activation of the Nrf2-ARE pathway via inhibition of 26S proteasome serves as part of a cellular defense mechanism to protect against paraquat toxicity. Expand
Dopamine facilitates alpha-synuclein oligomerization in human neuroblastoma SH-SY5Y cells.
TLDR
It is confirmed that stable overexpression of alpha-synuclein in SH-SY5Y cells indeed increased the amounts ofalpha-synucin oligomers in these cells and exposure of the cells to dopamine for 6h facilitated alpha- Synuclein oligomerization, and the dopamine-treated cells did not undergo cell death or apoptosis in spite of the presence of increased oligomeric alpha- synuclein. Expand
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