Glatiramer acetate protects against oxygen-glucose deprivation/reperfusion-induced injury by inhibiting Egr-1 in H9c2 cells

2020 ◽  
Vol 120 ◽  
pp. 61-66
Author(s):  
Jian Du ◽  
Wei Lv ◽  
Sitong Yang ◽  
Jia Liu ◽  
Juan Zhen ◽  
...  
Keyword(s):  
Glatiramer Acetate ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
H9c2 Cells

scholarly journals Plant Natural Product Formononetin Protects Rat Cardiomyocyte H9c2 Cells against Oxygen Glucose Deprivation and Reoxygenation via Inhibiting ROS Formation and Promoting GSK-3βPhosphorylation

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Yuanyuan Cheng ◽  
Zhengyuan Xia ◽  
Yifan Han ◽  
Jianhui Rong
Keyword(s):  
Natural Product ◽  
Glycogen Synthase ◽  
Ischemia Reperfusion ◽  
Membrane Integrity ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Dependent Manner ◽  
H9c2 Cells ◽  
Mptp Opening ◽  
Ros Formation

The opening of mitochondrial permeability transition pore (mPTP) is a major cause of cell death in ischemia reperfusion injury. Based on our pilot experiments, plant natural product formononetin enhanced the survival of rat cardiomyocyte H9c2 cells during oxygen glucose deprivation (OGD) and reoxygenation. For mechanistic studies, we focused on two major cellular factors, namely, reactive oxygen species (ROS) and glycogen synthase kinase 3β(GSK-3β), in the regulation of mPTP opening. We found that formononetin suppressed the formation of ROS and superoxide in a concentration-dependent manner. Formononetin also rescued OGD/reoxygenation-induced loss of mitochondrial membrane integrity. Further studies suggested that formononetin induced Akt activation and GSK-3β(Ser9) phosphorylation, thereby reducing GSK-3βactivity towards mPTP opening. PI3K and PKC inhibitors abolished the effects of formononetin on mPTP opening and GSK-3βphosphorylation. Immunoprecipitation experiments further revealed that formononetin increased the binding of phosphor-GSK-3βto adenine nucleotide translocase (ANT) while it disrupted the complex of ANT with cyclophilin D. Moreover, immunofluorescence revealed that phospho-GSK-3β(Ser9) was mainly deposited in the space between mitochondria and cell nucleus. Collectively, these results indicated that formononetin protected cardiomyocytes from OGD/reoxygenation injury via inhibiting ROS formation and promoting GSK-3βphosphorylation.

scholarly journals Knockdown of circular RNA circMAT2B reduces oxygen-glucose deprivation-induced inflammatory injury in H9c2 cells through up-regulating miR-133

Cell Cycle ◽  
2020 ◽  
Vol 19 (20) ◽  
pp. 2622-2630
Author(s):  
Yanhui Zhu ◽  
Chengwei Zou ◽  
Yanting Jia ◽  
Haizhou Zhang ◽  
Xiaochun Ma ◽  
...  
Keyword(s):  
Glucose Deprivation ◽  
Circular Rna ◽  
Oxygen Glucose Deprivation ◽  
H9c2 Cells ◽  
Inflammatory Injury

scholarly journals Cardioprotective Effect of Propofol against Oxygen Glucose Deprivation and Reperfusion Injury in H9c2 Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Dandan Zhao ◽  
Qing Li ◽  
Qiuping Huang ◽  
Xuguang Li ◽  
Min Yin ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Underlying Mechanism ◽  
Oxygen Glucose Deprivation ◽  
H9c2 Cell ◽  
Dependent Manner ◽  
H9c2 Cells

Background. The intravenous anesthetic propofol is reported to be a cardioprotective agent against ischemic-reperfusion injury in the heart. However, the regulatory mechanism still remains unclear.Methods. In this study, we used H9c2 cell line under condition of oxygen glucose deprivation (OGD) followed by reperfusion (OGD/R) to inducein vitrocardiomyocytes ischemia-reperfusion injury. Propofol (5, 10, and 20 μM) was added to the cell cultures before and during the OGD/R phases to investigate the underlying mechanism.Results. Our data showed that OGD/R decreased cell viability, and increased lactate dehydrogenase leakage, and reactive oxygen species and malondialdehyde production in H9c2 cells, all of which were significantly reversed by propofol. Moreover, we found that propofol increased both the activities and protein expressions of superoxide dismutase and catalase. In addition, propofol increased FoxO1 expression in a dose-dependent manner and inhibited p-AMPK formation significantly.Conclusions. These results indicate that the propofol might exert its antioxidative effect through FoxO1 in H9c2 cells, and it has a potential therapeutic effect on cardiac disorders involved in oxidative stress.

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