Abstract:
AIMS:Transition metals, oxidative stress and neuroinflammation have been proposed as part of a vicious cycle in central nervous system neurodegeneration. Our aim was to study the anti-inflammatory effect of pioglitazone, a peroxisome proliferative activated receptor-γ agonist, on iron-induced oxidative injury in rat brain. METHODS:Intranigral infusion of ferrous citrate (iron) was performed on anaesthetized rats. Pioglitazone (20 mg/kg) was orally administered. Oxidative injury was investigated by measuring lipid peroxidation in the substantia nigra (SN) and dopamine content in the striatum. Western blot assay and DNA fragmentation were employed to study the involvement of α-synuclein aggregation, neuroinflammation as well as activation of endoplasmic reticulum (ER) and mitochondrial pathways in iron-induced apoptosis. RESULTS:Intranigral infusion of iron time-dependently increased α-synuclein aggregation and haem oxygenase-1 levels. Furthermore, apoptosis was demonstrated by TUNEL-positive cells and DNA fragmentation in the iron-infused SN. Systemic pioglitazone was found to potentiate iron-induced elevation in nuclear peroxisome proliferative activated receptor-γ levels. However, pioglitazone inhibited iron-induced α-synuclein aggregation, elevations in interleukin-1β and interleukin-6 mRNA levels as well as increases in oxygenase-1, cyclo-oxygenase II, nitric oxide synthase and ED-1 protein levels, an indicator of activated microglia. Moreover, iron-induced DNA laddering as well as activation of ER and mitochondrial pathways were attenuated by pioglitazone. In addition, pioglitazone decreased iron-induced elevation in lipid peroxidation in the infused SN and depletion in striatal dopamine level. CONCLUSIONS:Our results suggest that pioglitazone prevents iron-induced apoptosis via both ER and mitochondrial pathways. Furthermore, inhibition of α-synuclein aggregation and neuroinflammation may contribute to the pioglitazone-induced neuroprotection in central nervous system.
journal_name
Neuropathol Appl Neurobioljournal_title
Neuropathology and applied neurobiologyauthors
Yu HC,Feng SF,Chao PL,Lin AMdoi
10.1111/j.1365-2990.2010.01107.xsubject
Has Abstractpub_date
2010-12-01 00:00:00pages
612-22issue
7eissn
0305-1846issn
1365-2990pii
NAN1107journal_volume
36pub_type
杂志文章abstract::Dystrophic (D) and normal (N) chicken pectoral muscle was analysed for histopathological differences from the embryo (day 20) through to the mature adult stage. A variety of indices of structural changes were used, to express the progression quantitatively. At the embryonic stage, fibroblast numbers (but not satellite...
journal_title:Neuropathology and applied neurobiology
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doi:10.1111/j.1365-2990.1983.tb00332.x
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abstract::To confirm the intracellular accumulation of amyloid beta-protein (Abeta), we carefully performed immunohistochemistry using brains of cynomolgus monkeys of various ages. Cortical neurones and their large neurites were immunostained with antibodies against Abeta in young monkey brains. In aged monkey brains, intracell...
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journal_title:Neuropathology and applied neurobiology
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journal_title:Neuropathology and applied neurobiology
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journal_title:Neuropathology and applied neurobiology
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journal_title:Neuropathology and applied neurobiology
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doi:10.1111/j.1365-2990.1989.tb01145.x
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abstract::Apoptotic bodies are frequently found in oligodendrogliomas, particularly in the anaplastic subtype. A range of proteins, such as those of the Bcl family, are implicated in the control of apoptosis. The ratio of antagonists of apoptosis, such as Bcl-2, to agonists, such as Bax, is thought to determine the outcome for ...
journal_title:Neuropathology and applied neurobiology
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journal_title:Neuropathology and applied neurobiology
pub_type: 杂志文章
doi:10.1111/j.1365-2990.1991.tb00738.x
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pub_type: 杂志文章
doi:10.1111/j.1365-2990.1988.tb00865.x
更新日期:1988-01-01 00:00:00
abstract::Defects of mitochondrial function have been proposed as a potential mechanism in the development and pathogenesis of Alzheimer's disease (AD) and neuronal apoptosis. Mitochondrial enzyme-deficient pyramidal neurones are found in greater quantities in the hippocampus of AD patients than in age-matched controls. The pre...
journal_title:Neuropathology and applied neurobiology
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更新日期:2002-10-01 00:00:00
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更新日期:2005-08-01 00:00:00
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journal_title:Neuropathology and applied neurobiology
pub_type: 杂志文章
doi:10.1111/j.1365-2990.1995.tb01027.x
更新日期:1995-02-01 00:00:00
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journal_title:Neuropathology and applied neurobiology
pub_type: 杂志文章
doi:10.1111/j.1365-2990.1996.tb01114.x
更新日期:1996-08-01 00:00:00
abstract::Two cases are described, one with a multifocal cranial and limb neuropathy of adult onset associated with optic neuropathy, and the other with a diffuse demyelinating neuropathy characterized by congenital cataract, mental retardation and progressive lower limb paresis with an onset in childhood. Extensive investigati...
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doi:10.1046/j.0305-1846.2000.00289.x
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pub_type: 杂志文章
doi:10.1111/j.1365-2990.1991.tb00748.x
更新日期:1991-12-01 00:00:00
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pub_type: 杂志文章
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journal_title:Neuropathology and applied neurobiology
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更新日期:2018-04-01 00:00:00
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更新日期:2014-10-01 00:00:00
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journal_title:Neuropathology and applied neurobiology
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doi:10.1111/j.1365-2990.1983.tb00111.x
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abstract::The pattern of cell loss and neuronal degeneration resulting from multiple microinjections of N-methyl-D-aspartate (NMDA), ibotenate (IBO), quisqualate (QUIS), and kainate (KA) into hippocampus was studied, together with the protection provided by the NMDA antagonist 3-(+/-)-2-carboxypiperazin-4-yl-propyl-1-phosphonat...
journal_title:Neuropathology and applied neurobiology
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更新日期:1993-10-01 00:00:00
abstract:AIMS:Oxidative damage and an associated DNA damage response (DDR) are evident in mild cognitive impairment and early Alzheimer's disease, suggesting that neuronal dysfunction resulting from oxidative DNA damage may account for some of the cognitive impairment not fully explained by Alzheimer-type pathology. METHODS:Fr...
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journal_title:Neuropathology and applied neurobiology
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doi:10.1111/j.1365-2990.1991.tb00693.x
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abstract::The brain is vulnerable to a number of acute insults, with traumatic brain injury being among the commonest. Neuroinflammation is a common response to acute injury and microglial activation is a key component of the inflammatory response. In the acute and subacute phase it is likely that this response is protective an...
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更新日期:2000-04-01 00:00:00