Role of nuclear factor-κB in a rat model of vascular injury

2001 ◽  
Vol 364 (4) ◽  
pp. 343-350 ◽  
Author(s):  
Armando Ialenti ◽  
Angela Ianaro ◽  
Pasquale Maffia ◽  
Rosa Carnuccio ◽  
Fulvio D'Acquisto ◽  
...  
Keyword(s):  
Vascular Injury ◽  
Rat Model ◽  
Nuclear Factor Κb ◽  
Nuclear Factor

The effect of curcumin on liver fibrosis in the rat model of microsurgical cholestasis

2015 ◽  
Vol 6 (7) ◽  
pp. 2187-2193 ◽  
Author(s):  
Andrej Barta ◽  
Pavol Janega ◽  
Pavel Babál ◽  
Erich Murár ◽  
Martina Cebová ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Liver Fibrosis ◽  
Inducible Nitric Oxide Synthase ◽  
Rat Model ◽  
Early Stage ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

We aimed to determine the effects of curcumin on liver fibrosis and to clarify the role of nuclear factor-κB (NF-κB) and inducible nitric oxide synthase (iNOS) in a model of microsurgical cholestasis in the early stage of extrahepatic biliary atresia.

ROLE OF NUCLEAR FACTOR κB IN MELANOMA PROGRESSION.

2007 ◽  
Vol 55 (1) ◽  
pp. S158
Author(s):  
A. M. DeLuca ◽  
B. Ryu ◽  
R. Alani
Keyword(s):  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Melanoma Progression

Role of nuclear factor-κB in gastric ulcer healing in rats

2001 ◽  
Vol 280 (6) ◽  
pp. G1296-G1304 ◽  
Author(s):  
Satoru Takahashi ◽  
Takuya Fujita ◽  
Akira Yamamoto
Keyword(s):  
Gastric Ulcer ◽  
Mrna Expression ◽  
Ulcer Healing ◽  
Nuclear Factor Κb ◽  
Normal Mucosa ◽  
Cyclooxygenase 2 ◽  
Interleukin 1Β ◽  
Nuclear Factor ◽  
Gastric Ulcer Healing

We investigated the role of nuclear factor-κB (NF-κB) in gastric ulcer healing in rats. NF-κB was activated in ulcerated tissue but not in normal mucosa, and the level of the activation was decreased with ulcer healing. NF-κB activation was observed in fibroblasts, monocytes/macrophages, and neutrophils. Treatment of gastric fibroblasts, isolated from the ulcer base, with interleukin-1β activated NF-κB and the subsequently induced cyclooxygenase-2 and cytokine-induced neutrophil chemoattractant-1 (CINC-1) mRNA expression. Inhibition of activated NF-κB action resulted in suppression of both their mRNA expression and increases in PGE2 and CINC-1 levels induced by interleukin-1β. Persistent prevention of NF-κB activation caused an impairment of ulcer healing in rats. Gene expression of interleukin-1β, CINC-1, cyclooxygenase-2, and inducible nitric oxide synthase in ulcerated tissue had been inhibited before the delay in ulcer healing became manifest. The increased levels of cyclooxygenase-2 protein and PGE2 production were also reduced. These results demonstrate that NF-κB, activated in ulcerated tissue, might upregulate the expression of healing-promoting factors responsible for gastric ulcer healing in rats.

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