Abstract:
:Microglia are known to be a primary inflammatory cell type in the brain. However, microglial inflammatory responses are attenuated in the injured brain compared to those in cultured pure microglia. In the present study, we found that astrocytes challenged by oxygen-glucose deprivation (OGD) or H(2) O(2) released soluble factor(s) and attenuated microglial inflammatory responses. Conditioned medium prepared from astrocytes treated with OGD (OGD-ACM) or H(2) O(2) (H(2) O(2) -ACM) significantly reduced the levels of interferon-γ (IFN-γ)-induced microglial inflammatory mediators, including inducible nitric oxide synthase, at both the mRNA and protein levels. The anti-inflammatory effect of astrocytes appeared very rapidly (within 5min), but was not closely correlated with the extent of astrocyte damage. Both OGD-ACM and H(2) O(2) -ACM inhibited STAT nuclear signaling, as evidenced by a reduction in both STAT-1/3 binding to the IFN-γ-activated site and IFN-γ-activated site promoter activity. However, both phosphorylation and nuclear translocation of STAT-1/3 was unchanged in IFN-γ-treated microglia. The active component(s) in OGD-ACM were smaller than 3kDa, and displayed anti-inflammatory effects independent of protein synthesis. These results suggest that, in the injured brain, astrocytes may act as a controller to rapidly suppress microglial activation.
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Kim JH,Min KJ,Seol W,Jou I,Joe EHdoi
10.1111/j.1471-4159.2010.07004.xsubject
Has Abstractpub_date
2010-12-01 00:00:00pages
1161-71issue
5eissn
0022-3042issn
1471-4159journal_volume
115pub_type
杂志文章abstract::Topiramate (TPM) is a structurally novel broad-spectrum anticonvulsant known to modulate the activity of several ligand- and voltage-gated ion channels in neurons. These include an inhibitory effect on the AMPA and kainate subtypes of glutamate receptors, mixed modulatory effects (usually positive) on some types of GA...
journal_title:Journal of neurochemistry
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1111/j.1471-4159.1991.tb08186.x
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journal_title:Journal of neurochemistry
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doi:10.1111/j.1471-4159.1982.tb06660.x
更新日期:1982-06-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1111/j.1471-4159.2008.05669.x
更新日期:2008-11-01 00:00:00
abstract::α-Synuclein causes Parkinson's disease if mutated or aberrantly produced in neurons. α-Synuclein-lipid interactions are important for the normal function of the protein, but can also contribute to pathogenesis. We previously reported that deletion of the first 10 N-terminal amino acids dramatically reduced lipid bindi...
journal_title:Journal of neurochemistry
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pub_type: 杂志文章
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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更新日期:1984-08-01 00:00:00
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pub_type: 杂志文章
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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更新日期:2012-04-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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更新日期:2000-11-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章,评审
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更新日期:2017-06-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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更新日期:1986-08-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1046/j.1471-4159.2001.00109.x
更新日期:2001-02-01 00:00:00
abstract::Three forms of acetylcholinesterase (AChE) have been reported: the 4S, 10S, and 16S forms. It was suggested previously that 16S AChE is characteristic of the end-plate region; subsequently its presence has also been demonstrated in sciatic nerve, vagus nerve, several nerve trunks, cardiac atria, and distal ileum of ra...
journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1111/j.1471-4159.1982.tb10882.x
更新日期:1982-01-01 00:00:00