We previously found that oxygen-glucose-serum deprivation/restoration（OGSD/R） induces apoptosis of spinal cord astrocytes, possibly via caspase-12 and the integrated stress response, which involves protein kinase R-like endoplasmic reticulum kinase（PERK）, eukaryotic initiation factor 2-alpha（eIF2α） and activating transcription factor 4（ATF4）. We hypothesized that edaravone, a low molecular weight, lipophilic free radical scavenger, would reduce OGSD/R-induced apoptosis of spinal cord astrocytes.... 

【文章來源】：Neural Regeneration Research. 2017,12(02)SCICSCD

【文章頁數(shù)】：7 頁

【文章目錄】：
Graphical Abstract
Introduction
Materials and Methods
    Animals
    Primary culture of spinal cord astrocytes
    Cell viability assay
    Apoptotic assay
    ROS
    Immunostaining
    Western blot assay
    Statistical analysis
Results
    Edaravone inhibited OGSD/R-induced apoptosis of astrocytes in rat spinal cord
    Edaravone inhibitd the release of ROS after OGSD/R
    Edaravone reduced caspase-12 protein expression after OGSD/R
    Edaravone reduced the expression of CHOP after OGSD/R
    Edaravone reduced expression of p-PERK,p-e IF2α,and ATF4 after OGSD/R
Discussion


【參考文獻(xiàn)】：
期刊論文
[1]Attenuation of endoplasmic reticulum stress as a treatment strategy against ischemia/reperfusion injury[J]. Chih-Li Lin.  Neural Regeneration Research. 2015(12)
[2]From adaption to death: endoplasmic reticulum stress as a novel target of selective neurodegeneration?[J]. Yiting Liu,James R.Connor.  Neural Regeneration Research. 2015(09)
[3]Neuroprotective effects of atorvastatin against cerebral ischemia/reperfusion injury through the inhibition of endoplasmic reticulum stress[J]. Jian-wen Yang,Zhi-ping Hu.  Neural Regeneration Research. 2015(08)



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