scholarly journals Hydrodynamics-based transfection of plasmid encoding receptor activator for nuclear factor kappa B-Fc protects against hepatic ischemia/reperfusion injury in mice

2010 ◽  
Vol 16 (5) ◽  
pp. 611-620 ◽  
Author(s):  
Jian Shi ◽  
Wenyu Shao ◽  
Dongchang Yang ◽  
Liang Zhao ◽  
Lei Deng ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Nuclear Factor Kappa B ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nuclear Factor ◽  
Hepatic Ischemia ◽  
Nuclear Factor Kappa ◽  
Receptor Activator ◽  
Hepatic Ischemia Reperfusion

scholarly journals Receptor activator of nuclear factor-κB ligand (RANKL) protects against hepatic ischemia/reperfusion injury in mice

Hepatology ◽  
2012 ◽  
Vol 55 (3) ◽  
pp. 888-897 ◽  
Author(s):  
Nozomu Sakai ◽  
Heather L. Van Sweringen ◽  
Rebecca Schuster ◽  
John Blanchard ◽  
Justin M. Burns ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Hepatic Ischemia ◽  
Receptor Activator ◽  
Hepatic Ischemia Reperfusion

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.

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