scholarly journals Impact of antioxidative treatment on nuclear factor kappa-B regulation during myocardial ischemia-reperfusion

2006 ◽  
Vol 5 (5) ◽  
pp. 531-535 ◽  
Author(s):  
U. M. Fischer
Keyword(s):  
Myocardial Ischemia ◽  
Nuclear Factor Kappa B ◽  
Ischemia Reperfusion ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Myocardial Ischemia Reperfusion ◽  
Antioxidative Treatment

scholarly journals Dexmedetomidine Preconditioning Protects Rats from Renal Ischemia–Reperfusion Injury Accompanied with Biphasic Changes of Nuclear Factor-Kappa B Signaling

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Naren Bao ◽  
Bing Tang ◽  
Junke Wang
Keyword(s):  
Reperfusion Injury ◽  
Nuclear Factor Kappa B ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Renal Ischemia Reperfusion Injury ◽  
Anti Inflammatory

Acute kidney injury (AKI) is one of the most common and troublesome perioperative complications. Dexmedetomidine (DEX) is a potent α2-adrenoceptor (α2-AR) agonist with anti-inflammatory and renoprotective effects. In this study, a rat renal ischemia–reperfusion injury (IRI) model was induced. At 24 h after reperfusion, the IRI-induced damage and the renoprotection of DEX preconditioning were confirmed both biochemically and histologically. Changes in nuclear factor-kappa B (NF-κB), as well as its downstream anti-inflammatory factor A20 and proinflammatory factor tumor necrosis factor-α (TNF-α), were detected. Atipamezole, a nonselective antagonist, was then added 5 min before the administration of DEX to further analyze DEX’s effects on NF-κB, and another anti-inflammatory medicine, methylprednisolone, was used in comparison with DEX, to further analyze DEX’s effects on NF-κB. Different concentrations of DEX (0 nM, 0.1 nM, 1 nM, 10 nM, 100 nM, 1 μM, and 10 μM) were applied to preincubated human renal tubular epithelial cell line (HK-2) cells in vitro. After anoxia and reoxygenation, the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) tetrazolium assay and enzyme-linked immunosorbent assay (ELISA) were performed to evaluate the levels of NF-κB downstream anti-inflammatory cytokines. The results showed that, unlike methylprednisolone, DEX preconditioning led to a time-dependent biphasic change (first activation then inhibition) of NF-κB in the rat renal IRI models that were given 25 μg/kg i.p. It was accompanied by a similarly biphasic change of TNF-α and an early and persistent upregulation of A20. In vitro, DEX’s cellular protection showed a concentration-dependent biphasic change which was protective within the range of 0 to 100 nM but became opposite when concentrations are greater than 1 μM. The changes in the A20 and NF-κB messenger RNA (mRNA) levels were consistent with the renoprotective ability of DEX. In other words, DEX preconditioning protected the rats from renal IRI via regulation biphasic change of NF-κB signaling.

Design and Development of Novel 1,3,5-Triazine-Procaine Derivatives as Protective Agent against Myocardial Ischemia/Reperfusion Injury via Inhibitor of Nuclear Factor-κB

Pharmacology ◽  
2019 ◽  
Vol 104 (3-4) ◽  
pp. 126-138
Author(s):  
Zhe Qiang ◽  
Wenli Yu ◽  
Yonghao Yu
Keyword(s):  
Myocardial Ischemia ◽  
Protective Effect ◽  
Hydroxyl Radical ◽  
Superoxide Anion ◽  
Ischemia Reperfusion ◽  
Nuclear Factor Κb ◽  
Treated Group ◽  
Nuclear Factor ◽  
Triazine Derivatives ◽  
Myocardial Ischemia Reperfusion

The aim of the present study was to determine the protective effect of novel 1,3,5-triazine-procaine derivatives against myocardial ischemia/reperfusion (I/R) injury. Initially, the experiment has been started by the synthesis of procaine, which later got substituted with diverse 1,3,5-triazine derivatives to furnish the final compounds. The target compounds were tested for nuclear factor-κB (NF-κB) inhibitory activity in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. The antioxidant activity of most potent compound 9i was investigated using hydroxyl radical, DPPH, and superoxide anion scavenging assay. Compound 9i was further evaluated for protective effect against myocardial I/R injury on the basis numerous parameters, for example, hemodynamic parameters (left ventricular developed pressure [LVDP], ±dp/dtmax, coronary flow [CF], and heart rate [HR]), myocardial enzymes (creatine kinase and lactate dehydrogenase), thiobarbituric acid reactive substance (TBARS), oxidative stress (super oxide dismutase [SOD], catalase [CAT], glutathione [GSH], and glutathione peroxidise [GPx]), histopathology, western blots analysis for B-cell lymphoma 2 (Bcl-2), Bcl-2-associated x protein (Bax), lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), and NF-κB in cardiac tissues. Compounds showed significant inhibition of NF-ĸB transcriptional activity in LPS-stimulated RAW264.7 cells, revealing compound 9i as a most potent derivative. In vitro results showed efficient reduction of reduced hydroxyl radical, DPPH, and superoxide anion by 9i. The level LVDP, ±dp/dtmax, CF, HR, TBARS, SOD, CAT, GSH, GPx, and damaged cardiac histopathology were completely restored to normal in 9i-treated group, as compared to I/R group. In western blot analysis, the expression of Bax, LOX-1, and NF-ĸB was found to be decreased, while the level of Bcl-2 was found to be increased in 9i-treated group. The procaine-1,3,5-triazine derivatives showed significant cardioprotective action via inhibition of NF-ĸB.

scholarly journals Protective Effects of Cinnamaldehyde against Mesenteric Ischemia-Reperfusion-Induced Lung and Liver Injuries in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Marwan Almoiliqy ◽  
Jin Wen ◽  
Eskandar Qaed ◽  
Yuchao Sun ◽  
Mengqiao Lian ◽  
...  
Keyword(s):  
Mesenteric Ischemia ◽  
Nuclear Factor Kappa B ◽  
Nuclear Translocation ◽  
Ischemia Reperfusion ◽  
Nuclear Factor ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Nuclear Factor Kappa ◽  
Liver Injuries ◽  
Liver Tissues

The aim of this study was to characterize and reveal the protective effects of cinnamaldehyde (CA) against mesenteric ischemia-reperfusion- (I/R-) induced lung and liver injuries and the related mechanisms. Sprague-Dawley (SPD) rats were pretreated for three days with 10 or 40 mg/kg/d, ig of CA, and then induced with mesenteric ischemia for 1 h and reperfusion for 2 h. The results indicated that pretreatment with 10 or 40 mg/kg of CA attenuated morphological damage in both lung and liver tissues of mesenteric I/R-injured rats. CA pretreatment significantly restored the levels of aspartate transaminase (AST) and alanine transaminase (ALT) in mesenteric I/R-injured liver tissues, indicating the improvement of hepatic function. CA also significantly attenuated the inflammation via reducing myeloperoxidase (MOP) activity and downregulating the expression of inflammation-related proteins, including interleukin-6 (IL-6), interleukin-1β (IL-1β), cyclooxygenase-2 (Cox-2), and tumor necrosis factor receptor type-2 (TNFR-2) in both lung and liver tissues of mesenteric I/R-injured rats. Pretreatment with CA significantly downregulated nuclear factor kappa B- (NF-κB-) related protein expressions (NF-κB p65, NF-κB p50, I kappa B alpha (IK-α), and inhibitor of nuclear factor kappa-B kinase subunit beta (IKKβ)) in both lung and liver tissues of mesenteric I/R-injured rats. CA also significantly downregulated the protein expression of p53 family members, including caspase-3, caspase-9, Bax, and p53, and restored Bcl-2 in both lung and liver tissues of mesenteric I/R-injured rats. CA pretreatment significantly reduced TUNEL-apoptotic cells and significantly inhibited p53 and NF-κB p65 nuclear translocation in both lung and liver tissues of mesenteric I/R-injured rats. CA neither induced pulmonary and hepatic histological alterations nor affected the parameters of inflammation and apoptosis in sham rats. We conclude that CA alleviated mesenteric I/R-induced pulmonary and hepatic injuries via attenuating apoptosis and inflammation through inhibition of NF-κB and p53 pathways in rats, suggesting the potential role of CA in remote organ ischemic injury protection.

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...

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