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dc.contributor.authorShakib, Nader-
dc.contributor.authorKhadem Ansari, Mohammad Hassan-
dc.contributor.authorKarimi, Pouran-
dc.contributor.authorRasmi, Yousef-
dc.description.abstractThe purpose of this study was to clarify the mechanisms of the protective effects of low-dose sodium nitrite (SN) on oxygen and glucose deprivation (OGD)-induced endoplasmic reticulum (ER) stress in PC12 cells. The PC12 cells were exposed to 4 h of OGD and treated with 100 μmol SN. The expression and activity of ER stress markers, including PKR-like endoplasmic reticulum kinase (PERK), transcription factor 6 (ATF6), CCAAT/enhancer binding protein homologous protein (CHOP), as well as caspase-12 and -3, were detected by immunoblotting assay. Fluorescence staining was used to detect the levels of reactive oxygen species (ROS) and Ca2+ release from the ER. Cell viability was also evaluated by MTT assay. It was found that SN significantly inhibited ROS production and Ca2+ release from the ER in OGD-injured PC12 cells. Moreover, ER stress marker expression and cleaved fragments of caspase-3 and -12 in OGD-injured PC12 cells were decreased after SN treatment. These findings were accompanied by a significant increase in cell viability. It seems that SN exerts a neuroprotective effect at least partially through reduction of ROS-mediated ER stress caused by OGD insult.en
dc.relation.ispartofseriesEXCLI Journal;Vol. 18 2019-
dc.subjectSodium nitriteen
dc.subjectOxygen and glucose deprivationen
dc.subjectPC12 cellsen
dc.subjectEndoplasmic reticulum stressen
dc.subjectCa2+ releaseen
dc.titleNeuroprotective mechanism of low-dose sodium nitrite in oxygen-glucose deprivation model of cerebral ischemic stroke in PC12 cellsen
dcterms.accessRightsopen access-
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