Differential effects of selective and non-selective inhibition of nitric oxide synthase on the expression and activity of cyclooxygenase-2 during gastric ulcer healing

2006 ◽  
Vol 536 (3) ◽  
pp. 301-308 ◽  
Author(s):  
Jin Sheng Guo ◽  
Chi Hin Cho ◽  
Ji Yao Wang ◽  
Marcel Wing Leung Koo
1998 ◽  
Vol 27 ◽  
pp. S64-S73 ◽  
Author(s):  
Yasutada Akiba ◽  
Masahiko Nakamura ◽  
Mikiji Mori ◽  
Hidekazu Suzuki ◽  
Masaya Oda ◽  
...  

2000 ◽  
Vol 279 (2) ◽  
pp. G341-G346 ◽  
Author(s):  
Li Ma ◽  
John L. Wallace

Nitric oxide has been shown to be beneficial for gastric ulcer healing. We determined the relative effects of endothelial and inducible nitric oxide synthases on gastric ulcer healing in rats. Ulcers were induced by serosal application of acetic acid. Ulcer severity, angiogenesis, and nitric oxide synthase expression were assessed 3–10 days later. The effects of inhibitors of nitric oxide synthase were also examined. Inducible nitric oxide synthase mRNA was only detected in ulcerated tissue (maximal at day 3), whereas the endothelial isoform mRNA was detected in normal tissue and increased during ulcer healing. Inducible nitric oxide synthase was expressed in inflammatory cells in the ulcer bed, whereas endothelial nitric oxide synthase was found in the vascular endothelium and in some mucosal cells in both normal and ulcerated tissues. Angiogenesis changed in parallel with endothelial nitric oxide synthase expression. N 6-(iminoethyl)-l-lysine did not affect angiogenesis or ulcer healing, while N G-nitro-l-arginine methyl ester significantly reduced both. In conclusion, endothelial nitric oxide synthase, but not the inducible isoform, plays a significant role in gastric ulcer healing.


2006 ◽  
Vol 6 (11) ◽  
pp. 1723-1728 ◽  
Author(s):  
José Antonio Guerra ◽  
María Francisca Molina ◽  
María José Abad ◽  
Angel María Villar ◽  
Paulina Bermejo

2002 ◽  
Vol 442 (1-2) ◽  
pp. 125-135 ◽  
Author(s):  
Bettina Berenguer ◽  
Catalina Alarcón de la Lastra ◽  
Francisco Javier Moreno ◽  
Maria José Martı́n

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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