scholarly journals Immune‐Responsive Gene 1/Itaconate Activates Nuclear Factor Erythroid 2–Related Factor 2 in Hepatocytes to Protect Against Liver Ischemia–Reperfusion Injury

Hepatology ◽  
2020 ◽  
Vol 72 (4) ◽  
pp. 1394-1411 ◽  
Author(s):  
Zhongjie Yi ◽  
Meihong Deng ◽  
Melanie J. Scott ◽  
Guang Fu ◽  
Patricia A. Loughran ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Related Factor ◽  
Nuclear Factor ◽  
Liver Ischemia ◽  
Responsive Gene

Sestrin2 is involved in Nrf2-regulated antioxidative signaling pathway in luteolin-induced prevention of the diabetic rat heart from ischemia/reperfusion injury

2021 ◽  
Author(s):  
Xin-Ru Zhou ◽  
Xiao-Chen Ru ◽  
Chi Xiao ◽  
Jie Pan ◽  
Yang-Yun Lou ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Rat Heart ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Rat ◽  
Related Factor ◽  
Nuclear Factor ◽  
Inducible Protein ◽  
Myocardial Ischemia Reperfusion

Luteolin attenuates myocardial ischemia/reperfusion (I/R) injury in diabetes through activating nuclear factor erythroid 2-related factor 2 (Nrf2)-related antioxidative response. Though sestrin2, a highly conserved stress-inducible protein, is regarded as a...

Argon reduces microglia activation and ramification dependent inflammatory cytokine expression in the retina

2019 ◽  
Author(s):  
Ulrich Goebel ◽  
Stefanie Scheid ◽  
Sashko Spassov ◽  
Nils Schallner ◽  
Jakob Wollborn ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Neuronal Damage ◽  
Noble Gas ◽  
Ischemia Reperfusion ◽  
Microglia Activation ◽  
Related Factor ◽  
Nuclear Factor ◽  
Human Neuroblastoma

Abstract Background: Perioperative damage of neuronal tissue due to insufficient cerebral circulation as a result of hypotension or stroke, lead to permanent destruction and functional impairment via apoptotic and inflammatory pathways. Recently, the noble gas argon has been shown to exert neuroprotective effects. Despite intensive research, the exact mechanism remains unclear. Methods: In-vitro, after injury of human neuroblastoma cells with rotenone over a period of four hours, postconditioning with argon 75 Vol% was performed for 2. In-vivo, retinal ischemia reperfusion injury in the rat was induced by increasing intraocular pressure for 1 hour (h). Upon reperfusion, argon was administered by inhalation for 2 h. Results: In summary, argon reduced binding activity of transcription factors involved in regulation of neuronal damage such as STAT3 (Signal transducer and activator of transcription 3), NF-kB (Nuclear factor `kappa-light-chain-enhancer´ of activated B-cells), AP-1 (Activator protein 1) and Nrf-2 (Nuclear factor erythroid 2-related factor 2). Flow cytometry analysis showed that argon down-regulated the Fas-Ligand. Since some of these transcription factors were regulated via toll-like receptors (TLR), their effects could be eliminated - at least in part - by OxPAPC (TLR2 and -4 inhibitor). Argon was able to reduce the quantity and the activity of neuronal microglia after ischemia-reperfusion injury. Consecutively, qPCR (quantitative Polymerase chain reaction) showed a reduction of the pro-inflammatory cytokines IL-1α (Interleukin-1α), IL-1ß (Interleukin-1ß), IL-6 (Interleukin 6), TNFα (Tumor necrosis factor alpha) and iNOS (inducible Nitric oxide synthase). Conclusion: Argon reduced the extent of inflammation after neuronal injury by suppression of transcription factors crucial for microglia activation. The therapeutic use of the noble gas would be ideal for treating in the context of neuronal damage due to the lack of known side effects and narcotic properties with preservation of neurological assessability. Although preclinical studies are promising, further investigations are required before argon can be approved for use in patients.

Kelch-like ECH-associated Protein 1-dependent Nuclear Factor-E2–related Factor 2 Activation in Relation to Antioxidation Induced by Sevoflurane Preconditioning

2017 ◽  
Vol 126 (3) ◽  
pp. 507-521 ◽  
Author(s):  
Min Cai ◽  
Li Tong ◽  
Beibei Dong ◽  
Wugang Hou ◽  
Likai Shi ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Small Interfering Rna ◽  
Nuclear Translocation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Related Factor ◽  
Nuclear Factor ◽  
Sevoflurane Preconditioning ◽  
Interfering Rna

Abstract Background The authors have reported that antioxidative effects play a crucial role in the volatile anesthetic-induced neuroprotection. Accumulated evidence shows that endogenous antioxidation could be up-regulated by nuclear factor-E2–related factor 2 through multiple pathways. However, whether nuclear factor-E2–related factor 2 activation is modulated by sevoflurane preconditioning and, if so, what is the signaling cascade underlying upstream of this activation are still unknown. Methods Sevoflurane preconditioning in mice was performed with sevoflurane (2.5%) 1 h per day for five consecutive days. Focal cerebral ischemia/reperfusion injury was induced by middle cerebral artery occlusion. Expression of nuclear factor-E2–related factor 2, kelch-like ECH-associated protein 1, manganese superoxide dismutase, thioredoxin-1, and nicotinamide adenine dinucleotide phosphate quinolone oxidoreductase-1 was detected (n = 6). The antioxidant activities and oxidative product expression were also examined. To determine the role of kelch-like ECH-associated protein 1 inhibition-dependent nuclear factor-E2–related factor 2 activation in sevoflurane preconditioning-induced neuroprotection, the kelch-like ECH–associated protein 1-nuclear factor-E2–related factor 2 signal was modulated by nuclear factor-E2–related factor 2 knockout, kelch-like ECH-associated protein 1 overexpression lentivirus, and kelch-like ECH-associated protein 1 deficiency small interfering RNA (n = 8). The infarct volume, neurologic scores, and cellular apoptosis were assessed. Results Sevoflurane preconditioning elicited neuroprotection and increased nuclear factor-E2–related factor 2 nuclear translocation, which in turn up-regulated endogenous antioxidation and reduced oxidative injury. Sevoflurane preconditioning reduced kelch-like ECH-associated protein 1 expression. Nuclear factor-E2–related factor 2 ablation abolished neuroprotection and reversed sevoflurane preconditioning by mediating the up-regulation of antioxidants. Kelch-like ECH-associated protein 1 overexpression reversed nuclear factor-E2–related factor 2 up-regulation and abolished the neuroprotection induced by sevoflurane preconditioning. Kelch-like ECH-associated protein 1 small interfering RNA administration improved nuclear factor-E2–related factor 2 expression and the outcome of mice subjected to ischemia/reperfusion injury. Conclusions Kelch-like ECH-associated protein 1 down-regulation–dependent nuclear factor-E2–related factor 2 activation underlies the ability of sevoflurane preconditioning to activate the endogenous antioxidant response, which elicits its neuroprotection.

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