Signal transduction through nuclear factor kappa B in ischemia-reperfusion and heart failure

2004 ◽  
Vol 99 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Guro Valen
Keyword(s):  
Heart Failure ◽  
Signal Transduction ◽  
Nuclear Factor Kappa B ◽  
Ischemia Reperfusion ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa

Dysregulated nuclear factor kappa B (NF-kB) dependent apoptosis predicts a point of functional no return in hypertrophic heart failure

2008 ◽  
Vol 207 (3) ◽  
pp. S28
Author(s):  
Nancy C. Moss ◽  
Peter Charles ◽  
Ru-hang Tang ◽  
Monte Willis ◽  
William E. Stansfield ◽  
...  
Keyword(s):  
Heart Failure ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa

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.

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.

scholarly journals Modulation of both activator protein-1 and nuclear factor-kappa B signal transduction of human T cells by amiodarone

2014 ◽  
Vol 240 (1) ◽  
pp. 99-108 ◽  
Author(s):  
Shu-Meng Cheng ◽  
Wei-Hsiang Lin ◽  
Chin-Sheng Lin ◽  
Ling-Jun Ho ◽  
Tsung-Neng Tsai ◽  
...  
Keyword(s):  
Signal Transduction ◽  
T Cells ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Activator Protein 1 ◽  
Activator Protein ◽  
Nuclear Factor Kappa ◽  
Human T Cells
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