[Effect of recombinant human trefoil factor on protection of gastric mucosa and healing of chronic gastric ulcer in rats].
Xiuyun Dong, Liya Zhou, Sanren Lin, Binggen Ru, Min Fang
Abstract
Xiuyun Dong, Liya Zhou, Sanren Lin, Binggen Ru, Min Fang
Abstract
OBJECTIVE: To study the effect of recombinant human intestinal trefoil factor ( rhITF) on the healing of rat chronic gastric ulcer, protect gastric mucosal and mechanisms are involved. METHODS: (1) Acute gastric mucosal injury was induced by ethanol, stress, aspirin and pylorusl ligation. The injury index,MDA, GMBL,hexosamine (Hex) and acid output were measure. (2) Chronic gastric ulcer was induced in rats by application of 50% glacial acetic acid to the serosa of the glandular stomach. After injury, rats received by rhITF or vehicle orally twice daily for 11 days. On day 12, gastric mucosal blood flow GMBF was measured under ether anesthesia. Then the pylorus was ligated for 3 hours and each stomach removed. The gastric acid output, ulcer index, Hex and nitric oxide(NO) content in gastric mucosa, as well as iNOSmRNA in the ulcer bed were determined. RESULTS: (1) rhITF protected gastric mucosa from the acute lesion, and increased Hex content in gastric mucosa. (2) rhITF treatment significantly decreased the ulcer index and gastric acid output, but increased the GMBF, Hex and NO content in comparison with the control groups. In addition, rhITF also stimulated iNOSmRNA expression in the ulcer bed by situ hybridization analysis. CONCLUSION: rhITF can protect gastric mucosa against acute lesion, and enhance the healing of chronic gastric ulcer in the rats. This action may result from the inhibition of gastric acid output, increase of GMBF.Hex and NO content and rhITF stimulated iNOSmRNA expression.
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OBJECTIVE: To study the effect of recombinant human intestinal trefoil factor ( rhITF) on the healing of rat chronic gastric ulcer, protect gastric mucosal and mechanisms are involved. METHODS: (1) Acute gastric mucosal injury was induced by ethanol, stress, aspirin and pylorusl ligation. The injury index,MDA, GMBL,hexosamine (Hex) and acid output were measure. (2) Chronic gastric ulcer was induced in rats by application of 50% glacial acetic acid to the serosa of the glandular stomach. After injury, rats received by rhITF or vehicle orally twice daily for 11 days. On day 12, gastric mucosal blood flow GMBF was measured under ether anesthesia. Then the pylorus was ligated for 3 hours and each stomach removed. The gastric acid output, ulcer index, Hex and nitric oxide(NO) content in gastric mucosa, as well as iNOSmRNA in the ulcer bed were determined. RESULTS: (1) rhITF protected gastric mucosa from the acute lesion, and increased Hex content in gastric mucosa. (2) rhITF treatment significantly decreased the ulcer index and gastric acid output, but increased the GMBF, Hex and NO content in comparison with the control groups. In addition, rhITF also stimulated iNOSmRNA expression in the ulcer bed by situ hybridization analysis. CONCLUSION: rhITF can protect gastric mucosa against acute lesion, and enhance the healing of chronic gastric ulcer in the rats. This action may result from the inhibition of gastric acid output, increase of GMBF.Hex and NO content and rhITF stimulated iNOSmRNA expression.
Key concepts: Gastric mucosa, Ulcer index, Medicine, Stomach, Gastroenterology, Internal medicine, Pylorus, Lesion