Neuroprotective mechanism of low-dose sodium nitrite in oxygen-glucose deprivation model of cerebral ischemic stroke in PC12 cells

EXCLI Journal

Nader Shakib¹  Mohammad Hassan Khadem Ansari²  Pouran Karimi³ 

[1] Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran;Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran, E-mail: [e-mail];Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran, E-mail: [e-mail]

关键词: sodium nitrite;    oxygen and glucose deprivation;    PC12 cells;    endoplasmic reticulum stress;    Ca2release;   

DOI  :  10.17179/excli2018-1947

学科分类：过敏症与临床免疫学

来源: University of Mainz, University of Leipzig

【 摘 要 】

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.

【 授权许可】

CC BY