Impaired gastric ulcer healing in diabetic rats: Role of angiogenesis, growth factors, heat shock protein and proinflammatory cytokines

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Tomasz Bizozowski auKarolina^Bazela ◽  
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pp. 249-260 ◽  
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Stanislaw J. Konturek ◽  
Vitaly Kukharsky ◽  
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2011 ◽  
Vol 82 (7) ◽  
pp. 728-736 ◽  
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Tomoaki Ishihara ◽  
Shintaro Suemasu ◽  
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Ken-ichiro Tanaka ◽  
Tohru Mizushima

2015 ◽  
Vol 60 (4) ◽  
pp. 850-857 ◽  
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Toshiharu Sakurai ◽  
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Satoru Hagiwara ◽  
Naoshi Nishida ◽  
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...  

2018 ◽  
Vol 6 (5) ◽  
pp. 01 ◽  
Author(s):  
Ajayi Ayodeji Folorunsho ◽  
Aniviye Blessing Oluwafunke ◽  
Kehinde Busuyi David ◽  
Akintola Adebola Olayemi

2001 ◽  
Vol 280 (6) ◽  
pp. G1296-G1304 ◽  
Author(s):  
Satoru Takahashi ◽  
Takuya Fujita ◽  
Akira Yamamoto

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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