scholarly journals Corrigendum: Propofol Alleviates DNA Damage Induced by Oxygen Glucose Deprivation and Reperfusion via FoxO1 Nuclear Translocation in H9c2 Cells

2020 ◽  
Vol 11 ◽  
Author(s):  
Dandan Zhou ◽  
Jinqiang Zhuang ◽  
Yihui Wang ◽  
Dandan Zhao ◽  
Lidong Zhao ◽  
...  
Keyword(s):  
Dna Damage ◽  
Nuclear Translocation ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
H9c2 Cells

Inhibition of N-myc Downstream–regulated Gene-2 Is Involved in an Astrocyte-specific Neuroprotection Induced by Sevoflurane Preconditioning

2014 ◽  
Vol 121 (3) ◽  
pp. 549-562 ◽  
Author(s):  
Xin Li ◽  
Peng Luo ◽  
Feng Wang ◽  
Qianzi Yang ◽  
Yan Li ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Glucose Deprivation ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Oxygen Glucose Deprivation ◽  
Ndrg2 Expression ◽  
Sevoflurane Preconditioning ◽  
Cellular Apoptosis ◽  
Cerebral Ischemic ◽  
Interfering Rna

Abstract Background: Mechanism of sevoflurane preconditioning–induced cerebral ischemic tolerance is unclear. This study investigates the role of N-myc downstream–regulated gene-2 (NDRG2) in the neuroprotection of sevoflurane preconditioning in ischemic model both in vivo and in vitro. Methods: At 2 h after sevoflurane (2%) preconditioning for 1 h, rats were subjected to middle cerebral artery occlusion for 120 min. Neurobehavioral scores (n = 10), infarct volumes (n = 10), cellular apoptosis (n = 6), and NDRG2 expression (n = 6) were determined at 24 h after reperfusion. In vitro, cultural astrocytes were exposed to oxygen–glucose deprivation for 4 h. Cellular viability, cytotoxicity, apoptosis, and NDRG2 expression (n = 6) were evaluated in the presence or absence of NDRG2-specific small interfering RNA or NDRG2 overexpression plasmid. Results: Sevoflurane preconditioning decreased apoptosis (terminal deoxynucleotidyl transferase–mediated 2’-deoxyuridine 5’-triphosphate nick-end labeling–positive cells reduced to 31.2 ± 5.3% and cleaved Caspase-3 reduced to 1.42 ± 0.21 fold) and inhibited NDRG2 expression (1.28 ± 0.15 fold) and nuclear translocation (2.21 ± 0.29 fold) in ischemic penumbra. Similar effects were observed in cultural astrocytes exposed to oxygen–glucose deprivation. NDRG2 knockdown by small interfering RNA attenuated oxygen–glucose deprivation–induced injury (cell viability increased to 80.5 ± 4.1%; lactate dehydrogenase release reduced to 30.5 ± 4.0%) and cellular apoptosis (cleaved Caspase-3 reduced to 1.55 ± 0.21 fold; terminal deoxynucleotidyl transferase–mediated 2’-deoxyuridine 5’-triphosphate nick-end labeling–positive cells reduced to 18.2 ± 4.3%), whereas NDRG2 overexpression reversed the protective effects of sevoflurane preconditioning. All the data are presented as mean ± SD. Conclusion: Sevoflurane preconditioning inhibits NDRG2 up-regulation and nuclear translocation in astrocytes to induce cerebral ischemic tolerance via antiapoptosis, which represents one new mechanism of sevoflurane preconditioning and provides a novel target for neuroprotection.

scholarly journals Neuroprotective Effects of Pycnogenol Against Oxygen-Glucose Deprivation/Reoxygenation-Induced Injury in Primary Rat Astrocytes via NF-κB and ERK1/2 MAPK Pathways

2017 ◽  
Vol 42 (3) ◽  
pp. 987-998 ◽  
Author(s):  
Ruixue Xia ◽  
Chunxue Ji ◽  
Leguo Zhang
Keyword(s):  
Inflammatory Cytokines ◽  
Nuclear Translocation ◽  
Cell Activity ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Neuroprotective Effects ◽  
Tnf Α ◽  
Anti Oxidant ◽  
Rat Astrocytes ◽  
Related Proteins

Backgrounds/Aims: Pycnogenol (PYC) is a patented mix of bioflavonoids with potent anti-oxidant and anti-inflammatory properties. In this study, we investigated the effects of PYC on oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury in primary rat astrocytes. Methods: The primary rat astrocytes were randomly divided into 6 groups, blank control, OGD/R, OGD/R+PYC (10, 20, 40, and 60 µg/mL). The cell activity were detected by MTT and LDH assays, then the levels of oxidant products [malondialdehyde (MDA) and reactive oxygen species (ROS)] , antioxidants [superoxide dismutase (SOD)], mitochondrial membrane potential (MMP) and inflammatory cytokines were detected. In addition, the expression levels of apoptosis-related proteins (Bax, Bcl-2 and Cleaved caspase 3), proinflammatory factors (NF-κB p65), and p-ERK1/2 were measured by Western blot analysis. Results: The results showed that PYC incubation dose-dependently attenuated cell viability loss, LDH leakage, oxidative stress, inflammatory cytokines accumulation and cell apoptosis caused by OGD/R. Furthermore, PYC pretreatment dose-dependently suppressed OGD/R-induced NF-κB p65 nuclear translocation, NF-κB activity and ERK1/2 phosphorylation. Similarly to PYC, NF-κB inhibitor PDTC and ERK1/2 inhibitor PD098059 dramatically inhibited OGD/R-induced NF-κB activation, ERK1/2 phosphorylation, and ROS production, as well as TNF-α secretion. Conclusions: These findings revealed that PYC has neuroprotective effects against OGD/R-induced injury via NF-κB and ERK1/2 pathways in primary rat astrocytes.

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