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By J. Chai

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Furthermore, both H. , 2000). H. pylori and NSAIDs act synergistically through pathways of inflammation in the development of ulcers and in ulcer bleeding (Figure 2). 3 Antagonistic action between H. pylori and NSAIDs NSAIDs have bacteriostatic and bactericidal activity against H. , 2006). NSAIDs inhibit COX-1 and COX-2. This inhibition declines PG synthesis, while H. , 2000) so as to enhance PG syntheses. H. pylori accelerates healing of gastric ulcer induced by NSAIDs in rats due to that H. pylori stimulates the overexpression of COX-2 and the increase of PG synthesis, and consequently increases the production of vascular endothelial growth factor (VEGF) and the vascular proliferation.

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Pylori and mitochondrial changes in epithelial cells. The role of oxidative stress. Revista Española de Enfermedades Digestivas (Madrid), Vol. 102, No 1 (January), pp. 41-50, ISSN 1130-0108. Chang, L. (2008). The Role of Stress on Physiological Responses and Clinical Symptoms in Irritable Bowel Syndrome. 4, (June), pp. 299–312, ISSN 1566-5240. V. (1993). Alcohol and gastric acid secretion in humans. 6 (June), pp. 843–847, ISSN 0017-5749. H. (1993). Endogenous somatostatin inhibits histamine release from canine gastric mucosal cells in primary culture.

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