Indomethacin treatment during initial period of acetic acid-induced rat gastric ulcer healing promotes persistent polymorphonuclear cell-infiltration and increases future ulcer recurrence

1996 ◽  
Vol 41 (10) ◽  
pp. 2055-2061 ◽  
Author(s):  
Tetsuo Arakawa ◽  
Toshio Watanabe ◽  
Takashi Fukuda ◽  
Kazuhide Higuchi ◽  
Osamu Takaishi ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Gastric Ulcer ◽  
Ulcer Healing ◽  
Initial Period ◽  
Cell Infiltration ◽  
Ulcer Recurrence ◽  
Polymorphonuclear Cell ◽  
Gastric Ulcer Healing ◽  
Indomethacin Treatment

Alpha-Lipoic Acid Improves Acetic Acid-Induced Gastric Ulcer Healing in Rats

Inflammation ◽  
2008 ◽  
Vol 32 (1) ◽  
pp. 37-46 ◽  
Author(s):  
Berna Karakoyun ◽  
Meral Yüksel ◽  
Feriha Ercan ◽  
Can Erzik ◽  
Berrak Ç. Yeğen
Keyword(s):  
Acetic Acid ◽  
Gastric Ulcer ◽  
Lipoic Acid ◽  
Ulcer Healing ◽  
Alpha Lipoic Acid ◽  
Gastric Ulcer Healing

S1634 Alpha-Lipoic Acid Improves Acetic Acid-Induced Gastric Ulcer Healing in Rats

2008 ◽  
Vol 134 (4) ◽  
pp. A-239
Author(s):  
Berna Karakoyun ◽  
Meral Yuksel ◽  
Feriha Ercan ◽  
Can Erzik ◽  
Berrak C. Yegen
Keyword(s):  
Acetic Acid ◽  
Gastric Ulcer ◽  
Lipoic Acid ◽  
Ulcer Healing ◽  
Alpha Lipoic Acid ◽  
Gastric Ulcer Healing

scholarly journals Accelerated Ulcer Healing and Resistance to Ulcer Recurrence with Gastroprotectants in Rat Model of Acetic Acid-induced Gastric Ulcer

2008 ◽  
Vol 42 (3) ◽  
pp. 204-214 ◽  
Author(s):  
Tae Young Oh ◽  
Byung Ok Ahn ◽  
Eun Jung Jang ◽  
Joo Sang Park ◽  
Sang Jong Park ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Gastric Ulcer ◽  
Rat Model ◽  
Ulcer Healing ◽  
Ulcer Recurrence

Gastric ulcer healing is regulated by platelets through endostatin release: Modulation by ticlopidine, aspirin and celecoxib

2001 ◽  
Vol 120 (5) ◽  
pp. A143-A143
Author(s):  
L MA ◽  
S ELLIOTT ◽  
G CIRINO ◽  
A BURET ◽  
J WALLACE
Keyword(s):  
Gastric Ulcer ◽  
Ulcer Healing ◽  
Gastric Ulcer Healing

Gastric ulcer healing is regulated by platelets through endostatin release: Modulation by ticlopidine, aspirin and celecoxib

2001 ◽  
Vol 120 (5) ◽  
pp. A143
Author(s):  
Li Ma ◽  
Susan N. Elliott ◽  
Giuseppe Cirino ◽  
Andre Buret ◽  
John L. Wallace
Keyword(s):  
Gastric Ulcer ◽  
Ulcer Healing ◽  
Gastric Ulcer Healing

Chronic gastric ulcer healing in rats subjected to selective and non-selective cyclooxygenase-2 inhibitors

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

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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