Nuclear factor-κB p65 and upregulation of interleukin-6 in retinal ischemia/reperfusion injury in rats

2006 ◽  
Vol 1081 (1) ◽  
pp. 211-218 ◽  
Author(s):  
Jiantao Wang ◽  
Shaoyun Jiang ◽  
Jacky M.K. Kwong ◽  
Ruben N. Sanchez ◽  
Alfredo A. Sadun ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Interleukin 6 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nuclear Factor Κb ◽  
Retinal Ischemia ◽  
Nuclear Factor

Attenuation of lung reperfusion injury after transplantation using an inhibitor of nuclear factor-κB

2000 ◽  
Vol 279 (3) ◽  
pp. L528-L536 ◽  
Author(s):  
Scott D. Ross ◽  
Irving L. Kron ◽  
James J. Gangemi ◽  
Kimberly S. Shockey ◽  
Mark Stoler ◽  
...  
Keyword(s):  
Lung Function ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Graft Function ◽  
Nuclear Factor Κb ◽  
Pyrrolidine Dithiocarbamate ◽  
Nuclear Factor ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

A central role for nuclear factor-κB (NF-κB) in the induction of lung inflammatory injury is emerging. We hypothesized that NF-κB is a critical early regulator of the inflammatory response in lung ischemia-reperfusion injury, and inhibition of NF-κB activation reduces this injury and improves pulmonary graft function. With use of a porcine transplantation model, left lungs were harvested and stored in cold Euro-Collins preservation solution for 6 h before transplantation. Activation of NF-κB occurred 30 min and 1 h after transplant and declined to near baseline levels after 4 h. Pyrrolidine dithiocarbamate (PDTC), a potent inhibitor of NF-κB, given to the lung graft during organ preservation (40 mmol/l) effectively inhibited NF-κB activation and significantly improved lung function. Compared with control lungs 4 h after transplant, PDTC-treated lungs displayed significantly higher oxygenation, lower Pco2, reduced mean pulmonary arterial pressure, and reduced edema and cellular infiltration. These results demonstrate that NF-κB is rapidly activated and is associated with poor pulmonary graft function in transplant reperfusion injury, and targeting of NF-κB may be a promising therapy to reduce this injury and improve lung function.

Effect of a Novel Nuclear Factor-κB Activation Inhibitor on Renal Ischemia-Reperfusion Injury

2013 ◽  
Vol 96 (10) ◽  
pp. 863-870 ◽  
Author(s):  
Hidaka Kono ◽  
Ken Nakagawa ◽  
Shinya Morita ◽  
Kazunobu Shinoda ◽  
Ryuichi Mizuno ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nuclear Factor Κb ◽  
Renal Ischemia ◽  
Nuclear Factor ◽  
Renal Ischemia Reperfusion Injury

Interleukin-6 in Retinal Ischemia Reperfusion Injury in Rats

2003 ◽  
Vol 44 (9) ◽  
pp. 4006 ◽  
Author(s):  
Ruben N. Sanchez ◽  
Candy K. Chan ◽  
Sumit Garg ◽  
Jacky M. K. Kwong ◽  
Micheline J. Wong ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Interleukin 6 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Retinal Ischemia

scholarly journals Glycemia-dependent Nuclear Factor κB Activation Contributes to Mechanical Allodynia in Rats with Chronic Postischemia Pain

2013 ◽  
Vol 119 (3) ◽  
pp. 687-697 ◽  
Author(s):  
Marie-Christine Ross-Huot ◽  
André Laferrière ◽  
Mina Khorashadi ◽  
Terence J. Coderre
Keyword(s):  
Reperfusion Injury ◽  
Dorsal Horn ◽  
Mechanical Allodynia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nuclear Factor Κb ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Nuclear Factor ◽  
Normal Feeding

Abstract Background: Ischemia–reperfusion injury causes chronic postischemia pain (CPIP), and rats with higher glycemia during ischemia–reperfusion injury exhibit increased allodynia. Glycemia-induced elevation of nuclear factor κB (NFκB) may contribute to increased allodynia. Methods: Glycemia during a 3-h ischemia–reperfusion injury was manipulated by: normal feeding; or normal feeding with administration of insulin; dextrose; or insulin/dextrose. In these groups, NFκB was measured in ipsilateral hind paw muscle and spinal dorsal horn by enzyme-linked immunosorbent assay (ELISA), and SN50, an NFκB inhibitor, was administered to determine its differential antiallodynic effects depending on glycemia. Results: CPIP fed/insulin rats (12.03 ± 4.9 g, N = 6) had less allodynia than fed, fed/insulin/dextrose, and fed/dextrose rats (6.29 ± 3.37 g, N = 7; 4.57 ± 3.03 g, N = 6; 2.95 ± 1.10 g, N = 9), respectively. Compared with fed rats (0.209 ± 0.022 AU, N = 7), NFκB in ipsilateral plantar muscles was significantly lower for fed/insulin rats, and significantly higher for fed/dextrose rats (0.152 ± 0.053 AU, N = 6; 0.240 ± 0.057 AU, N = 7, respectively). Furthermore, NFκB in the dorsal horn of fed, fed/insulin/dextrose, and fed/dextrose rats (0.293 ± 0.049 AU; 0.267 ± 0.037 AU; 0.315 ± 0.015 AU, respectively, N = 6 for each) was significantly higher than in fed/insulin animals (0.267 ± 0.037 AU, N = 6). The antiallodynic SN50 dose–response curves of CPIP rats in the fed/insulin/dextrose, fed/dextrose, and fed conditions exhibited a rightward shift compared with the fed/insulin group. The threshold SN50 dose of CPIP fed/dextrose, fed/insulin/dextrose, and fed rats (328.94 ± 92.4 ng, 77.80 ± 44.50 ng, and 24.89 ± 17.20 ng, respectively) was higher than that for fed/insulin rats (4.06 ± 7.04 ng). Conclusions: NFκB was activated in a glycemia-dependent manner in CPIP rats. Hypoglycemic rats were more sensitive to SN50 than rats with higher glycemia. The finding that SN50 reduces mechanical allodynia suggests that NFκB inhibitors might be useful for treating postischemia pain.

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