<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Paintlia MK</submitter><funding>NCRR NIH HHS</funding><funding>NINDS NIH HHS</funding><pagination>956-70</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2659629</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>105(3)</volume><pubmed_abstract>Glial cells secrete proinflammatory mediators in the brain in response to exogenous stimuli such as infection and injury. Previously, we documented that systemic maternal lipopolysaccharide (LPS)-exposure at embryonic gestation day 18 causes oligodendrocyte (OL)-injury/hypomyelination in the developing brain which can be attenuated by N-acetyl cysteine (NAC; precursor of glutathione). The present study delineates the underlying mechanism of NAC-mediated attenuation of inhibition of OL development in LPS-stimulated mixed glial cultures. Factors released by LPS-stimulated mixed glial cultures inhibited OL development as shown by decrease in both proliferation 3bromo-deoxyuridine+/chondroitin sulfate proteoglycan-NG2+, hereafter BrdU+/NG+ and differentiation (O4+ and myelin basic protein+) of</pubmed_abstract><journal>Journal of neurochemistry</journal><pubmed_title>Modulation of peroxisome proliferator-activated receptor-alpha activity by N-acetyl cysteine attenuates inhibition of oligodendrocyte development in lipopolysaccharide stimulated mixed glial cultures.</pubmed_title><pmcid>PMC2659629</pmcid><funding_grant_id>R01 NS034741</funding_grant_id><funding_grant_id>R01 NS022576-17</funding_grant_id><funding_grant_id>R01 NS037766</funding_grant_id><funding_grant_id>C06 RR015455</funding_grant_id><funding_grant_id>NS-40810</funding_grant_id><funding_grant_id>R01 NS037766-10</funding_grant_id><funding_grant_id>NS-22576</funding_grant_id><funding_grant_id>R01 NS022576</funding_grant_id><funding_grant_id>R37 NS022576-24</funding_grant_id><funding_grant_id>NS-37766</funding_grant_id><funding_grant_id>NS-34741</funding_grant_id><funding_grant_id>C06 RR018823</funding_grant_id><funding_grant_id>R01 NS040810</funding_grant_id><funding_grant_id>R01 NS034741-12</funding_grant_id><funding_grant_id>R37 NS022576</funding_grant_id><pubmed_authors>Singh AK</pubmed_authors><pubmed_authors>Singh I</pubmed_authors><pubmed_authors>Khan M</pubmed_authors><pubmed_authors>Paintlia MK</pubmed_authors><pubmed_authors>Paintlia AS</pubmed_authors></additional><is_claimable>false</is_claimable><name>Modulation of peroxisome proliferator-activated receptor-alpha activity by N-acetyl cysteine attenuates inhibition of oligodendrocyte development in lipopolysaccharide stimulated mixed glial cultures.</name><description>Glial cells secrete proinflammatory mediators in the brain in response to exogenous stimuli such as infection and injury. Previously, we documented that systemic maternal lipopolysaccharide (LPS)-exposure at embryonic gestation day 18 causes oligodendrocyte (OL)-injury/hypomyelination in the developing brain which can be attenuated by N-acetyl cysteine (NAC; precursor of glutathione). The present study delineates the underlying mechanism of NAC-mediated attenuation of inhibition of OL development in LPS-stimulated mixed glial cultures. Factors released by LPS-stimulated mixed glial cultures inhibited OL development as shown by decrease in both proliferation 3bromo-deoxyuridine+/chondroitin sulfate proteoglycan-NG2+, hereafter BrdU+/NG+ and differentiation (O4+ and myelin basic protein+) of</description><dates><release>2008-01-01T00:00:00Z</release><publication>2008 May</publication><modification>2025-04-27T00:20:11.655Z</modification><creation>2019-06-06T21:20:51Z</creation></dates><accession>S-EPMC2659629</accession><cross_references><pubmed>18205750</pubmed><doi>10.1111/j.1471-4159.2007.05199.x</doi></cross_references></HashMap>