{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Paintlia MK"],"funding":["NCRR NIH HHS","NINDS NIH HHS"],"pagination":["956-70"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2659629"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["105(3)"],"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"],"journal":["Journal of neurochemistry"],"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."],"pmcid":["PMC2659629"],"funding_grant_id":["R01 NS034741","R01 NS022576-17","R01 NS037766","C06 RR015455","NS-40810","R01 NS037766-10","NS-22576","R01 NS022576","R37 NS022576-24","NS-37766","NS-34741","C06 RR018823","R01 NS040810","R01 NS034741-12","R37 NS022576"],"pubmed_authors":["Singh AK","Singh I","Khan M","Paintlia MK","Paintlia AS"],"additional_accession":[]},"is_claimable":false,"name":"Modulation of peroxisome proliferator-activated receptor-alpha activity by N-acetyl cysteine attenuates inhibition of oligodendrocyte development in lipopolysaccharide stimulated mixed glial cultures.","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","dates":{"release":"2008-01-01T00:00:00Z","publication":"2008 May","modification":"2025-04-27T00:20:11.655Z","creation":"2019-06-06T21:20:51Z"},"accession":"S-EPMC2659629","cross_references":{"pubmed":["18205750"],"doi":["10.1111/j.1471-4159.2007.05199.x"]}}