scholarly journals Age-related decrease in proteasome expression contributes to defective nuclear factor-κB activation during hepatic ischemia/reperfusion

Hepatology ◽  
2009 ◽  
Vol 49 (5) ◽  
pp. 1718-1728 ◽  
Author(s):  
Nadine Huber ◽  
Nozomu Sakai ◽  
Thorsten Eismann ◽  
Thomas Shin ◽  
Satoshi Kuboki ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Hepatic Ischemia ◽  
Age Related ◽  
Hepatic Ischemia Reperfusion

Effect of heat shock preconditioning on NF-κB/I-κB pathway during I/R injury of the rat liver

2002 ◽  
Vol 282 (6) ◽  
pp. G962-G971 ◽  
Author(s):  
Hiroshi Uchinami ◽  
Yuzo Yamamoto ◽  
Makoto Kume ◽  
Kei Yonezawa ◽  
Yasuhide Ishikawa ◽  
...  
Keyword(s):  
Heat Shock ◽  
Messenger Rna ◽  
Ischemia Reperfusion ◽  
Nuclear Factor Κb ◽  
Control Group ◽  
Nuclear Factor ◽  
Fatal Complication ◽  
Hepatic Ischemia ◽  
Proinflammatory Mediators ◽  
Hepatic Ischemia Reperfusion

Hepatic ischemia-reperfusion (I/R) injury continues to be a fatal complication after liver surgery. Heat shock (HS) preconditioning is an effective strategy for protecting the liver from I/R injury, but its exact mechanism is still unclear. Because the activation of nuclear factor-κB (NF-κB) is an important event in the hepatic I/R-induced inflammatory response, the effect of HS preconditioning on the pathway for NF-κB activation was investigated. In the control group, NF-κB was activated 60 min after reperfusion, but this activation was suppressed in the HS group. Messenger RNA expressions of proinflammatory mediators during reperfusion were also reduced with HS preconditioning. Concomitant with NF-κB activation, NF-κB inhibitor I-κB proteins were degraded in the control group, but this degradation was suppressed in the HS group. This study shows that HS preconditioning protected the liver from I/R injury by suppressing the activation of NF-κB and the subsequent expression of proinflammatory mediators through the stabilization of I-κB proteins.

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 The nuclear factor HMGB1 mediates hepatic injury after murine liver ischemia-reperfusion

2005 ◽  
Vol 201 (7) ◽  
pp. 1135-1143 ◽  
Author(s):  
Allan Tsung ◽  
Rohit Sahai ◽  
Hiroyuki Tanaka ◽  
Atsunori Nakao ◽  
Mitchell P. Fink ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
High Mobility ◽  
Neutralizing Antibody ◽  
Nuclear Factor Κb ◽  
Organ Damage ◽  
Dependent Manner ◽  
Nuclear Factor ◽  
Hepatic Ischemia ◽  
Murine Liver ◽  
Hepatic Ischemia Reperfusion

High-mobility group box 1 (HMGB1) is a nuclear factor that is released extracellularly as a late mediator of lethality in sepsis as well as after necrotic, but not apoptotic, death. Here we demonstrate that in contrast to the delayed role of HMGB1 in the systemic inflammation of sepsis, HMGB1 acts as an early mediator of inflammation and organ damage in hepatic ischemia reperfusion (I/R) injury. HMGB1 levels were increased during liver I/R as early as 1 h after reperfusion and then increased in a time-dependent manner up to 24 h. Inhibition of HMGB1 activity with neutralizing antibody significantly decreased liver damage after I/R, whereas administration of recombinant HMGB1 worsened I/R injury. Treatment with neutralizing antibody was associated with less phosphorylation of c-Jun NH2-terminal kinase and higher nuclear factor–κB DNA binding in the liver after I/R. Toll-like receptor 4 (TLR4)-defective (C3H/Hej) mice exhibited less damage in the hepatic I/R model than did wild-type (C3H/HeOuj) mice. Anti-HMGB1 antibody failed to provide protection in C3H/Hej mice, but successfully reduced damage in C3H/Ouj mice. Together, these results demonstrate that HMGB1 is an early mediator of injury and inflammation in liver I/R and implicates TLR4 as one of the receptors that is involved in the process.

scholarly journals Hyperglycemia Aggravates Hepatic Ischemia Reperfusion Injury by Inducing Chronic Oxidative Stress and Inflammation

2016 ◽  
Vol 2016 ◽  
pp. 1-16 ◽  
Author(s):  
Yihan Zhang ◽  
Dongdong Yuan ◽  
Weifeng Yao ◽  
Qianqian Zhu ◽  
Yue Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Nuclear Factor ◽  
Hepatic Ischemia ◽  
Chronic Oxidative Stress ◽  
Hepatic Ischemia Reperfusion ◽  
And Oxidative Stress

Aim. To investigate whether hyperglycemia will aggravate hepatic ischemia reperfusion injury (HIRI) and the underlying mechanisms.Methods. Control and streptozotocin-induced diabetic Sprague-Dawley rats were subjected to partial hepatic ischemia reperfusion. Liver histology, transferase, inflammatory cytokines, and oxidative stress were assessed accordingly. Similarly, BRL-3A hepatocytes were subjected to hypoxia/reoxygenation (H/R) after high (25 mM) or low (5.5 mM) glucose culture. Cell viability, reactive oxygen species (ROS), and activation of nuclear factor-erythroid 2-related factor 2 (Nrf2) and nuclear factor of kappa light polypeptide gene enhancer in B-cells (NF-κB) were determined.Results. Compared with control, diabetic rats presented more severe hepatic injury and increased hepatic inflammatory cytokines and oxidative stress. HIRI in diabetic rats could be ameliorated by pretreatment of N-acetyl-L-cysteine (NAC) or apocynin. Excessive ROS generation and consequent Nrf2 and NF-κB translocation were determined after high glucose exposure. NF-κB translocation and its downstream cytokines were further increased in high glucose cultured group after H/R. While proper regulation of Nrf2 to its downstream antioxidases was observed in low glucose cultured group, no further induction of Nrf2 pathway by H/R after high glucose culture was identified.Conclusion. Hyperglycemia aggravates HIRI, which might be attributed to chronic oxidative stress and inflammation and potential malfunction of antioxidative system.

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