Protective effect of nicotinamide on neuronal cells under oxygen and glucose deprivation and hypoxia/reoxygenation

2004 ◽  
Vol 11 (4) ◽  
pp. 472-481 ◽  
Author(s):  
Chiung-Chyi Shen ◽  
Hsueh-Meei Huang ◽  
Hsiu-Chung Ou ◽  
Huan-Lian Chen ◽  
Wen-Chi Chen ◽  
...  
Keyword(s):  
Protective Effect ◽  
Neuronal Cells ◽  
Glucose Deprivation ◽  
Oxygen And Glucose Deprivation ◽  
Hypoxia Reoxygenation

scholarly journals Comparative Study of the Effect of Baicalin and Its Natural Analogs on Neurons with Oxygen and Glucose Deprivation Involving Innate Immune Reaction of TLR2/TNFα

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Hui-Ying Li ◽  
Jun Hu ◽  
Shuang Zhao ◽  
Zhi-Yi Yuan ◽  
Hong-Jiao Wan ◽  
...  
Keyword(s):  
Protective Effect ◽  
Immune Reaction ◽  
Glucose Deprivation ◽  
Innate Immune ◽  
Oxygen Glucose Deprivation ◽  
Toll Like Receptor ◽  
Tlr2 Expression ◽  
Oxygen And Glucose Deprivation ◽  
Toll Like Receptor 2 ◽  
Anti Inflammation

This work is to study the baicalin and its three analogs, baicalin, wogonoside, and wogonin, on the protective effect of neuron from oxygen-glucose deprivation (OGD) and toll-like receptor 2 (TLR2) expression in OGD damage. The results showed that baicalin and its three analogs did protect neurons from OGD damage and downregulated protein level of TLR2. D-Glucopyranosiduronic acid on site 7 in the structure played a core of cytotoxicity of these flavonoid analogs. The methoxyl group on carbon 8 of the structure had the relation with TLR2 protein expression, as well as the anti-inflammation. In addition, we detected caspase3 and antioxidation capability, to investigate the effect of four analogs on cell apoptosis and total antioxidation competence in OGD model.

scholarly journals H2S protects hippocampal neurons against hypoxia-reoxygenation injury by promoting RhoA phosphorylation at Ser188

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Ye Chen ◽  
Jiyue Wen ◽  
Zhiwu Chen
Keyword(s):  
Endothelial Cells ◽  
Hippocampal Neurons ◽  
Glucose Deprivation ◽  
Rhoa Activity ◽  
Mercaptopyruvate Sulfurtransferase ◽  
Dependent Protein ◽  
Cerebral Vasodilatation ◽  
Reoxygenation Injury ◽  
Hypoxia Reoxygenation

AbstractInhibition of RhoA-ROCK pathway is involved in the H2S-induced cerebral vasodilatation and H2S-mediated protection on endothelial cells against oxygen-glucose deprivation/reoxygenation injury. However, the inhibitory mechanism of H2S on RhoA-ROCK pathway is still unclear. The aim of this study was to investigate the target and mechanism of H2S in inhibition of RhoA/ROCK. GST-RhoAwild and GST-RhoAS188A proteins were constructed and expressed, and were used for phosphorylation assay in vitro. Recombinant RhoAwild-pEGFP-N1 and RhoAS188A-pEGFP-N1 plasmids were constructed and transfected into primary hippocampal nerve cells (HNCs) to evaluate the neuroprotective mechanism of endothelial H2S by using transwell co-culture system with endothelial cells from cystathionine-γ-lyase knockout (CSE−/−) mice and 3-mercaptopyruvate sulfurtransferase knockout (3-MST−/−) rats, respectively. We found that NaHS, exogenous H2S donor, promoted RhoA phosphorylation at Ser188 in the presence of cGMP-dependent protein kinase 1 (PKG1) in vitro. Besides, both exogenous and endothelial H2S facilitated the RhoA phosphorylation at Ser188 in HNCs, which induced the reduction of RhoA activity and membrane transposition, as well as ROCK2 activity and expression. To further investigate the role of endothelial H2S on RhoA phosphorylation, we detected H2S release from ECs of CSE+/+ and CSE−/− mice, and 3-MST+/+ and 3-MST−/− rats, respectively, and found that H2S produced by ECs in the culture medium is mainly catalyzed by CSE synthase. Moreover, we revealed that both endothelial H2S, mainly catalyzed by CSE, and exogenous H2S protected the HNCs against hypoxia-reoxygenation injury via phosphorylating RhoA at Ser188.

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