Abstract

We have confirmed in our laboratory the antiulcer activity of curcumin during the acute chronic phase of gastric ulcer disease at doses of 20, 40 and 80 mg/kg (dissolved in saline solution). In the previous study, the potent effective dose of curcumin was 80 mg/kg that appears a propitious protective effect against gastric ulcer development. Therefore, the comparison between such recommended dose of curcumin and one of the proton pump inhibitors (PPIs) staff is worth-while. Since, the pharmacological control of gastric acid secretion is the main desired goal for gastro-cytoprotection, particularly, the H+/K+-ATPase (acid proton pump) inhibitors. Nevertheless, several studies have indicated that long-term inhibition of gastric acid secretion results in mucosal hyperplasia and carcinoid tumor development, due to increase circulating gastrin levels. Ulcer and the preventive indexes were scored, mucin, juice volume, total acidity, luminal haemoglobin, total antioxidant and total peroxide were evaluated. The pro-inflammatory cytokine IL-6 and the major angiogenic growth factor VEGF levels were measured. Conclusion, curcumin and omeprazole are potentially preventing gastric lesions development in the gastric wall during the acute phase of gastric ulcer diseases, but curcumin was more potent in its effect. Curcumin promotes gastric ulcer prevention/healing by induction of angiogenesis in the granular tissue of ulcers. That may be via upregulation of VEGF expression as reflected from VEGF level in serum and gastric juice, however, omeprazole might be has no role in this story.

Highlights

  • The prevention of gastric ulcer pathogenesis or its recurrence is the main desired goal for the clinical and the experimental studies in the present era

  • We have confirmed in our laboratory the antiulcer activity of curcumin during the acute chronic phase of gastric ulcer disease at doses of 20, 40 and 80 mg/kg

  • Impairment of gastric ulcer healing depends upon the increased release of proinflammatory cytokines and a decrease in the gastric mucosal blood flow and angiogenesis through reducing vascular endothelial cell growth factor (VEGF) expression [2]

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Summary

Introduction

The prevention of gastric ulcer pathogenesis or its recurrence is the main desired goal for the clinical and the experimental studies in the present era. Impairment of gastric ulcer healing depends upon the increased release of proinflammatory cytokines and a decrease in the gastric mucosal blood flow and angiogenesis through reducing vascular endothelial cell growth factor (VEGF) expression [2]. Mucins are heavily glycosylated glycoproteins that are the major components of the mucus viscous gel covering epithelial tissues. They form lubricants protective selective barrier on epithelial surfaces, and modulate cell-cell and cell-extracellular matrix interactions, lymphocyte trafficking and anti-immune recognition. Their expression is regulated by several cytokines and local and endocrine hormones [3,4,5].

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