Role of Oxidative Stress in Ischemia–Reperfusion-Induced Changes in Na+,K+-ATPase Isoform Expression in Rat Heart

2004 ◽  
Vol 6 (5) ◽  
pp. 914-923 ◽  
Author(s):  
Petr Ostadal ◽  
Adel B. Elmoselhi ◽  
Irena Zdobnicka ◽  
Anton Lukas ◽  
Vijayan Elimban ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Heart ◽  
Ischemia Reperfusion ◽  
Isoform Expression ◽  
Induced Changes

Role of Oxidative Stress in Ischemia–Reperfusion-Induced Changes in Na+,K+-ATPase Isoform Expression in Rat Heart

2004 ◽  
Vol 6 (5) ◽  
pp. 914-923 ◽  
Author(s):  
Petr Ostadal ◽  
Adel B. Elmoselhi ◽  
Irena Zdobnicka ◽  
Anton Lukas ◽  
Vijayan Elimban ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Heart ◽  
Ischemia Reperfusion ◽  
Isoform Expression ◽  
Induced Changes

The effect of oxidative stress on Na+K+ ATPase isoform expression in rat heart during ischemia-reperfusion

2002 ◽  
Vol 34 (6) ◽  
pp. A47
Author(s):  
Petr Ostadal ◽  
Adel B. Elmoselhi ◽  
Irena Zdobnicka ◽  
Donald Chapman ◽  
Mona Chappellaz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Heart ◽  
Ischemia Reperfusion ◽  
Isoform Expression

LncRNA SNHG12 Improves Cerebral Ischemic-reperfusion Injury by Activating SIRT1/FOXO3a Pathway through I nhibition of Autophagy and Oxidative Stress

2020 ◽  
Vol 17 (4) ◽  
pp. 394-401
Author(s):  
Yuanhua Wu ◽  
Yuan Huang ◽  
Jing Cai ◽  
Donglan Zhang ◽  
Shixi Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Cell Activity ◽  
Ht22 Cells ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Reperfusion ◽  
And Oxidative Stress

Background: Ischemia/reperfusion (I/R) injury involves complex biological processes and molecular mechanisms such as autophagy. Oxidative stress plays a critical role in the pathogenesis of I/R injury. LncRNAs are the regulatory factor of cerebral I/R injury. Methods: This study constructs cerebral I/R model to investigate role of autophagy and oxidative stress in cerebral I/R injury and the underline regulatory mechanism of SIRT1/ FOXO3a pathway. In this study, lncRNA SNHG12 and FOXO3a expression was up-regulated and SIRT1 expression was down-regulated in HT22 cells of I/R model. Results: Overexpression of lncRNA SNHG12 significantly increased the cell viability and inhibited cerebral ischemicreperfusion injury induced by I/Rthrough inhibition of autophagy. In addition, the transfected p-SIRT1 significantly suppressed the release of LDH and SOD compared with cells co-transfected with SIRT1 and FOXO3a group and cells induced by I/R and transfected with p-SNHG12 group and overexpression of cells co-transfected with SIRT1 and FOXO3 further decreased the I/R induced release of ROS and MDA. Conclusion: In conclusion, lncRNA SNHG12 increased cell activity and inhibited oxidative stress through inhibition of SIRT1/FOXO3a signaling-mediated autophagy in HT22 cells of I/R model. This study might provide new potential therapeutic targets for further investigating the mechanisms in cerebral I/R injury and provide.

scholarly journals Protective Role of Glutathione in the Hippocampus after Brain Ischemia

2021 ◽  
Vol 22 (15) ◽  
pp. 7765
Author(s):  
Youichirou Higashi ◽  
Takaaki Aratake ◽  
Takahiro Shimizu ◽  
Shogo Shimizu ◽  
Motoaki Saito
Keyword(s):  
Oxidative Stress ◽  
Neuronal Death ◽  
Excitatory Amino Acid ◽  
Ischemia Reperfusion ◽  
Thiol Group ◽  
Protective Role ◽  
Key Factor ◽  
Rate Limiting ◽  
Cysteine Uptake

Stroke is a major cause of death worldwide, leading to serious disability. Post-ischemic injury, especially in the cerebral ischemia-prone hippocampus, is a serious problem, as it contributes to vascular dementia. Many studies have shown that in the hippocampus, ischemia/reperfusion induces neuronal death through oxidative stress and neuronal zinc (Zn2+) dyshomeostasis. Glutathione (GSH) plays an important role in protecting neurons against oxidative stress as a major intracellular antioxidant. In addition, the thiol group of GSH can function as a principal Zn2+ chelator for the maintenance of Zn2+ homeostasis in neurons. These lines of evidence suggest that neuronal GSH levels could be a key factor in post-stroke neuronal survival. In neurons, excitatory amino acid carrier 1 (EAAC1) is involved in the influx of cysteine, and intracellular cysteine is the rate-limiting substrate for the synthesis of GSH. Recently, several studies have indicated that cysteine uptake through EAAC1 suppresses ischemia-induced neuronal death via the promotion of hippocampal GSH synthesis in ischemic animal models. In this article, we aimed to review and describe the role of GSH in hippocampal neuroprotection after ischemia/reperfusion, focusing on EAAC1.

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