Autor(en): | Shakib, Nader Khadem Ansari, Mohammad Hassan Karimi, Pouran Rasmi, Yousef |
Titel: | Neuroprotective mechanism of low-dose sodium nitrite in oxygen-glucose deprivation model of cerebral ischemic stroke in PC12 cells |
Sprache (ISO): | en |
Zusammenfassung: | The 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. |
Schlagwörter: | Sodium nitrite Oxygen and glucose deprivation PC12 cells Endoplasmic reticulum stress Ca2+ release |
URI: | http://hdl.handle.net/2003/38182 http://dx.doi.org/10.17877/DE290R-20161 |
Erscheinungsdatum: | 2019-04-08 |
Enthalten in den Sammlungen: | Original Articles |
Dateien zu dieser Ressource:
Datei | Beschreibung | Größe | Format | |
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Ansari_Karimi_08042019_proof.pdf | DNB | 485.17 kB | Adobe PDF | Öffnen/Anzeigen |
Ansari_Karimi_08042019_supplementary_data.pdf | DNB | 1.49 MB | Adobe PDF | Öffnen/Anzeigen |
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