Angiogenesis, cell proliferation and apoptosis in gastric ulcer healing. Effect of a selective cox-2 inhibitor

2004 ◽  
Vol 505 (1-3) ◽  
pp. 187-194 ◽  
Author(s):  
Susana Sánchez-Fidalgo ◽  
Inés Martín-Lacave ◽  
Matilde Illanes ◽  
Virginia Motilva
Author(s):  
Ari - Yuniarto

Objective: In the gastrointestinal system, gastric ulcer is one of the common serious problems in human life and gives contribution against morbidity and mortality incidence. The pathophysiology of gastric ulcer is an imbalance between aggressive factor and mucosal integrity factor. Increase of aggressive factors and decrease of mucosal integrity factors have potential against developed of gastric ulcer disease. The objective of the research was to evaluate antioxidant and gastric ulcer healing effect of Orthosiphon stamineus (Benth.) leaves extract in aspirin-induced rats.Methods: In vivo antiulcer activity of Orthosiphon leaves extract was evaluated through several parameters involves gastric acidity, number of ulcers, diameters of ulcers, ulcer index (UI), and healing ratio. Dose level of Orthosiphon leaves extract which used in this study such as 250 and500 mg/kg, respectively. Antioxidant activity of Orthosiphon leaves extract was evaluated by 1,1-diphenyl-2-picrylhydrazyl hydrate (DPPH) method. Histopathological of the stomach was performed using hematoxylin-eosin stained.Results: The results of the study showed that groups which given Orthosiphon leaves extract have significantly different for gastric ulcer healing compared to the control group and were supported by histopathological analysis. The Orthosiphon leaves extract also showed maximum scavengingactivity at a concentration of 100 µg/ml (58.86% inhibition) and minimum at 50 μg/ml (29.60% inhibition) with inhibitory concentration 50% (IC  )50 84.54 µg/ml when compared to ascorbic acid as the standard with IC5.08 µg/ml by DPPH method.Conclusion: It can be concluded that from the experimental study of O. stamineus (Benth.) leaves extract has potential antiulcer activity in aspirin- induced rats model and antioxidant effect using DPPH method. Stomach tissues regeneration in gastric ulcer model might be affected by the improvement of antioxidant status.Keywords: Orthosiphon stamineus (Benth.), Extract, Ulcer, Aspirin, 1,1-diphenyl-2-picrylhydrazyl hydrate.


2012 ◽  
Vol 44 (7) ◽  
pp. 565-576 ◽  
Author(s):  
A. Chatterjee ◽  
S. Chatterjee ◽  
S. Das ◽  
A. Saha ◽  
S. Chattopadhyay ◽  
...  

2011 ◽  
Vol 140 (5) ◽  
pp. S-318
Author(s):  
Andy Tau ◽  
David Graham ◽  
Waqar A. Qureshi ◽  
Hala El-Zimaity ◽  
Antone R. Opekun

2001 ◽  
Vol 120 (5) ◽  
pp. A598
Author(s):  
Catalina Alarcon de La Lastra ◽  
Bettina Berenguer ◽  
Virginia Motilva ◽  
Carmen La Casa ◽  
Juan Manuel Herrerias ◽  
...  

2004 ◽  
Vol 287 (2) ◽  
pp. G444-G451 ◽  
Author(s):  
Shuhei Miura ◽  
Atsushi Tatsuguchi ◽  
Ken Wada ◽  
Hiroki Takeyama ◽  
Yoko Shinji ◽  
...  

VEGF is a highly specific stimulator of endothelial cells and may play an important role in angiogenesis in the process of tissue regeneration. We previously showed that cyclooxygenase-2 (COX-2) expressed in mesenchymal cells of the ulcer bed is involved in the ulcer repair process. To clarify the role of COX-2 in angiogenesis during gastric ulcer healing, we investigated the relation between COX-2 expression and VEGF production in human gastric fibroblasts in vivo and in vitro. Gastric fibroblasts were cultured in RPMI 1640 with and without IL-1α or IL-1β in the presence or absence of NS-398, a selective COX-2 inhibitor. Supernatant VEGF and PGE2 concentrations were measured by enzyme-linked immunosorbent assay. COX-2 expression in fibroblasts was determined by Western blot analysis. VEGF and COX-2 expression in surgical resections of human gastric ulcer tissue was examined immunohistochemically. IL-1 dose dependently enhanced VEGF release in cultured gastric fibroblasts after a 24-h stimulation. IL-1 also stimulated PGE2 production in gastric fibroblasts via COX-2 induction. NS-398 significantly suppressed VEGF and PGE2 release from IL-1-stimulated gastric fibroblasts; concurrent addition of PGE2 restored NS-398-inhibited VEGF release. COX-2 and VEGF immunoreactivity were colocalized in fibroblast-like cells in the ulcer bed of gastric tissues. These results suggest that COX-2 plays a key role in VEGF production in gastric fibroblasts stimulated by IL-1 in vitro and that angiogenesis induced by the COX-2-VEGF pathway might be involved in gastric ulcer healing.


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