FoxO4 negatively modulates USP10 transcription to aggravate the apoptosis and oxidative stress of hypoxia/reoxygenation-induced cardiomyocytes by regulating the Hippo/YAP pathway

2021 ◽  
Author(s):  
Jingwen Huang ◽  
Yu Liu ◽  
Mei Wang ◽  
Rong Wang ◽  
Huifen Ling ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
And Oxidative Stress ◽  
Hypoxia Reoxygenation

scholarly journals Effects of neuroglobin overexpression on mitochondrial function and oxidative stress following hypoxia/reoxygenation in cultured neurons

2009 ◽  
Vol 87 (1) ◽  
pp. 164-170 ◽  
Author(s):  
Jianxiang Liu ◽  
Zhanyang Yu ◽  
Shuzhen Guo ◽  
Sun-Ryung Lee ◽  
Changhong Xing ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Function ◽  
Cultured Neurons ◽  
And Oxidative Stress ◽  
Hypoxia Reoxygenation

Etomidate Regulates miR-192-5p Expression to Reduce Hypoxia-Reoxygenation Induced Bronchial Epithelial Cell Damage

2021 ◽  
Vol 11 (3) ◽  
pp. 458-465
Author(s):  
Tian Xia ◽  
Yang Cao ◽  
Jinxiu Li ◽  
Xin Zhang ◽  
Guangyuan Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Protein Level ◽  
Cell Damage ◽  
Bronchial Epithelial Cells ◽  
Sod Activity ◽  
Bronchial Epithelial ◽  
Apoptosis Rate ◽  
And Oxidative Stress ◽  
Hypoxia Reoxygenation

Etomidate is a new type of intravenous anesthetic that can protect bronchial epithelial cells from oxidative stress damage. miR-192-5p is upregulated in 6-hydroxydopamine-induced neurocytes. This study explored the effect of etomidate on bronchial epithelial cell apoptosis and oxidative stress induced by hypoxia and reoxygenation and its regulatory effect on miR-192-5p. The human bronchial epithelial cells BEAS-2B were cultured in vitro and then subjected to hypoxia and reoxygenation to establish a cell injury model. The cells were then treated with etomidate at different doses. Moreover, anti-miR-NC and anti-miR-192-5p were transfected into the BEAS-2B cells to treat the hypoxia-reoxygenation. Moreover, miR-NC and miR-192-5p mimics were transfected into BEAS-2B cells, followed by treatment with 90 µmol/L etomidate for 24 h and then treatment with hypoxia and reoxygenation. The 2,4-dinitrophenylhydrazine method was used to determine the level of LDH in the culture medium of cardiomyocytes. Thiobarbituric acid was used to determine the level of MDA and xanthine oxidase to determine the activity of SOD. Flow cytometry was used to measure the apoptosis rate and qRT-PCR to evaluate miR-192-5p expression. Western blotting was used to determine the Bax and Bcl-2 protein levels. Compared with the findings in the control group, the levels of LDH and MDA, the apoptosis rate, and the protein level of Bax were increased (P < 0.05) upon treatment with hypoxia and reoxygenation, while SOD activity and Bcl-2 protein level were decreased (P < 0.05). In a manner dependent on the dose, etomidate could significantly reverse the effects of hypoxia and reoxygenation on oxidative stress and apoptosis of BEAS-2B cells (P < 0.05). Hypoxia and reoxygenation could significantly increase the miR-192-5p level of BEAS-2B cells (P < 0.05), while etomidate could reduce this miR-192-5p expression (P < 0.05) in a dose-dependent manner. Transfection of anti-miR-192-5p dramatically reduced LDH, MDA, apoptosis rate, and Bax protein level (P < 0.05), but was associated with increases of SOD activity and Bcl-2 protein expression (P < 0.05). High expression of miR-192-5p could significantly reverse the influence of etomidate on apoptosis and oxidative stress of BEAS-2B cells induced by hypoxia-reoxygenation (P < 0.05). Etomidate restrained the apoptosis of bronchial epithelial cells and oxidative stress induced by hypoxia and reoxygenation by inhibiting miR-192-5p expression, thereby reducing cell damage.

scholarly journals Scutellarin attenuates hypoxia/reoxygenation injury in hepatocytes by inhibiting apoptosis and oxidative stress through regulating Keap1/Nrf2/ARE signaling

2019 ◽  
Vol 39 (11) ◽  
Author(s):  
Haiyuan Wu ◽  
Lan Jia
Keyword(s):  
Oxidative Stress ◽  
Ischemia Reperfusion ◽  
Heme Oxygenase 1 ◽  
Oxygen Species ◽  
Protective Effects ◽  
Sod Activity ◽  
Reoxygenation Injury ◽  
Nrf2 Expression ◽  
And Oxidative Stress ◽  
Hypoxia Reoxygenation

Abstract Scutellarin is a natural flavonoid that has been found to exhibit anti-ischemic effect. However, the effect of scutellarin on hepatic hypoxia/reoxygenation (ischemia–reperfusion (I/R)) injury remains unknown. The aim of the present study was to explore the protective effect of scutellarin on I/R-induced injury in hepatocytes. Our results showed that scutellarin improved cell viability in hepatocytes exposed to hypoxia/reoxygenation (H/R). Scutellarin treatment resulted in decreased levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and increased superoxide dismutase (SOD) activity in H/R-induced hepatocytes. In addition, scutellarin reduced cell apoptosis in H/R-stimulated hepatocytes, as proved by the decreased apoptotic rate. Moreover, scutellarin significantly up-regulated bcl-2 expression and down-regulated bax expression in hepatocytes exposed to H/R. Furthermore, scutellarin treatment caused significant decrease in Keap1 expression and increase in nuclear Nrf2 expression. Besides, scutellarin induced the mRNA expressions of heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1). Inhibition of Nrf2 significantly reversed the protective effects of scutellarin on H/R-stimulated hepatocytes. In conclusion, these findings demonstrated that scutellarin protected hepatocytes from H/R-induced oxidative injury through regulating the Keap1/Nrf2/ARE signaling pathway, indicating a potential relevance of scutellarin in attenuating hepatic I/R injury.

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