scholarly journals Inhibition of nuclear factor-κB activation improves the survival of rats with taurocholate pancreatitis

Gut ◽  
1999 ◽  
Vol 44 (2) ◽  
pp. 253-258 ◽  
Author(s):  
A Satoh ◽  
T Shimosegawa ◽  
M Fujita ◽  
K Kimura ◽  
A Masamune ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Alveolar Macrophages ◽  
Fatal Outcome ◽  
Nuclear Factor Κb ◽  
Multiple Organ ◽  
Pyrrolidine Dithiocarbamate ◽  
Nuclear Factor ◽  
Taurocholate Pancreatitis ◽  
Severity Of The Disease

BackgroundDeath in the early stages of severe acute pancreatitis is frequently the result of multiple organ dysfunction, but its mechanism is not clear.AimsTo investigate the state of nuclear factor-κB (NF-κB) in macrophages of rats with lethal pancreatitis, and to assess the effectiveness of pyrrolidine dithiocarbamate, an inhibitor of NF-κB, on the pathology and mortality.MethodsTaurocholate pancreatitis was produced in rats, and the severity of the disease, the mortality, and activation of NF-κB in peritoneal and alveolar macrophages were compared in rats receiving pyrrolidine dithiocarbamate (PDTC) treatment and those that were not.ResultsTaurocholate pancreatitis produced massive necrosis, haemorrhage, and severe leucocyte infiltration in the pancreas as well as alveolar septal thickening in the lung. NF-κB was activated in peritoneal and alveolar macrophages six hours after pancreatitis induction. Pretreatment with PDTC dose-dependently attenuated the NF-κB activation and improved the survival of the rats, although it did not affect the early increase in serum amylase and histological findings.ConclusionsEarly blockage of NF-κB activation may be effective in reducing fatal outcome in severe acute pancreatitis.

scholarly journals Emodin has a protective effect in cases of severe acute pancreatitis via inhibition of nuclear factor-κB activation resulting in antioxidation

2014 ◽  
Vol 11 (2) ◽  
pp. 1416-1420 ◽  
Author(s):  
WEI-YAN YAO ◽  
YU-FEN ZHOU ◽  
AI-HUA QIAN ◽  
YONG-PING ZHANG ◽  
MIN-MIN QIAO ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Protective Effect ◽  
Severe Acute Pancreatitis ◽  
Nuclear Factor Κb ◽  
Nuclear Factor

scholarly journals Activation of nuclear factor-κB and intervention of NBD peptides in rats with severe acute pancreatitis

2008 ◽  
Vol 16 (18) ◽  
pp. 1980
Author(s):  
Wen-Rui Xie ◽  
Ken Chen ◽  
Xiao-Ya Yang ◽  
You-Ming Long ◽  
Hui Wang ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Nuclear Factor Κb ◽  
Nuclear Factor

Effects of Acupuncture at St25 on Inflammatory Mediators and Nuclear Factor κB Activation in a Rat Model of Severe Acute Pancreatitis

2015 ◽  
Vol 33 (4) ◽  
pp. 299-304 ◽  
Author(s):  
Qi-Ming Xue ◽  
Hui Pan ◽  
Lu Huang ◽  
Ning Li
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Inflammatory Mediators ◽  
Morphological Changes ◽  
Sodium Taurocholate ◽  
Serum Levels ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Sprague Dawley ◽  
Tnf Α

Objective To observe the effect of electroacupuncture (EA) and manual acupuncture (MA) at ST25 on inflammatory mediators and nuclear factor κ-B (NF-κB) activation in rats with sodium taurocholate-induced severe acute pancreatitis (SAP). Methods Eighty-eight male Sprague–Dawley rats were randomly divided into four groups: control (sham-operated), SAP, SAP+EA and SAP+MA (n=22 each). A SAP model was established by injecting 3.5% sodium taurocholate 1 mL/kg into the pancreatic duct. In each group, animals were killed at t=3 h (n=7), 6 h (n=7) and 12 h (n=8) after the procedure. Pancreatic expression of NF-κB was examined by immunohistochemical staining. The levels of tumour necrosis factor α (TNF-α) and interleukin 6 (IL-6) in serum were determined by ELISA. Pathological changes in the pancreas were examined microscopically. Results Serum levels of TNF-α and IL-6 increased and morphological changes consistent with tissue damage were observed in the pancreas of SAP rats. NF-κB p65 expression was significantly higher in the SAP group than in the sham-operated group (p<0.05). Treatment with acupuncture at ST25 attenuated morphological damage and reduced levels of TNF-α and IL-6 in serum. NF-κB p65 expression was also significantly reduced by acupuncture at ST25 in the pancreas at 6 and 12 h after the procedure (p<0.05). There were no significant differences between the SAP+EA and SAP+MA groups. Conclusions Acupuncture at ST25 might have a therapeutic effect on rats with SAP through inhibition of NF-κB expression and a reduction in the release of pro-inflammatory cytokines.

scholarly journals Activation of Nuclear Factor κB and Induction of Inducible Nitric Oxide Synthase by Ureaplasma urealyticumin Macrophages

2000 ◽  
Vol 68 (12) ◽  
pp. 7087-7093 ◽  
Author(s):  
Y.-H. Li ◽  
Z.-Q. Yan ◽  
J. Skov Jensen ◽  
K. Tullus ◽  
A. Brauner
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Alveolar Macrophages ◽  
Nuclear Factor Κb ◽  
Inos Expression ◽  
Dependent Manner ◽  
Nuclear Factor ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

ABSTRACT Chronic lung disease (CLD) of prematurity is an inflammatory disease with a multifactorial etiology. The importance ofUreaplasma urealyticum in the development of CLD is debated, and steroids produce some improvement in neonates with this disease. In the present study, the capability of U. urealyticum to stimulate rat alveolar macrophages to produce nitric oxide (NO), express inducible nitric oxide synthase (iNOS), and activate nuclear factor κB (NF-κB) in vitro was characterized. The effect of NO on the growth of U. urealyticum was also investigated. In addition, the impact of dexamethasone and budesonide on these processes was examined. We found that U. urealyticum antigen (≥4 × 107 color-changing units/ml) stimulated alveolar macrophages to produce NO in a dose- and time-dependent manner (P < 0.05). This effect was further enhanced by gamma interferon (100 IU/ml; P < 0.05) but was attenuated by budesonide and dexamethasone (10−4 to 10−6 M) (P < 0.05). The mRNA and protein levels of iNOS were also induced in response to U. urealyticum and inhibited by steroids.U. urealyticum antigen triggered NF-κB activation, a possible mechanism for the induced iNOS expression, which also was inhibited by steroids. NO induced by U. urealyticum caused a sixfold reduction of its own growth after infection for 10 h. Our findings imply that U. urealyticum may be an important factor in the development of CLD. The host defense response againstU. urealyticum infection may also be influenced by NO. The down-regulatory effect of steroids on NF-κB activation, iNOS expression, and NO production might partly explain the beneficial effect of steroids in neonates with CLD.

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.

Multiple organ dysfunction associated with severe acute pancreatitis (SAP)

2001 ◽  
Vol 120 (5) ◽  
pp. A644-A645
Author(s):  
Kimmo I. Halonen ◽  
Ville Pettila ◽  
Ari K. Leppaniemi ◽  
Esko A. Kemppainen ◽  
Pauli A. Puolakkainen ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Organ Dysfunction ◽  
Severe Acute Pancreatitis ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction

scholarly journals Inhibition of nuclear factor-κB activation by pyrrolidine dithiocarbamate prevents chronic FK506 nephropathy

2003 ◽  
Vol 63 (1) ◽  
pp. 306-314 ◽  
Author(s):  
Satoshi Tamada ◽  
Tatsuya Nakatani ◽  
Toshihiro Asai ◽  
Koichiro Tashiro ◽  
Toshiyuki Komiya ◽  
...  
Keyword(s):  
Nuclear Factor Κb ◽  
Pyrrolidine Dithiocarbamate ◽  
Nuclear Factor
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