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作 者:王立新[1] 林三仁[1] 董秀云[1] 杨雪玲[1] 周丽雅[1]
出 处:《胃肠病学》1999年第3期137-139,共3页Chinese Journal of Gastroenterology
摘 要:目的:研究铝碳酸镁对幽门结扎及乙醇诱发大鼠胃粘膜损伤的保护作用及其机制。方法:通过结扎幽门和灌服乙醇制备大鼠胃粘膜损伤模型,测定胃酸分泌、胃蛋白酶活性、胃粘膜中前列腺素、血流、丙二醛(MDA)、氨基己精含量和一些酶的活性。结果:口服铝碳酸镁500mg/kg连续3天,能显著防止幽门结扎和乙醇诱发的胃粘膜损伤,并中和胃酸及抑制胃蛋白酶活性。铝碳酸镁有促进前列腺素分泌和粘膜血流的作用。此外,铝碳酸镁能降低乙醇所致MDA含量的增加,并阻止乙醇引起的醌还原酶、谷胱甘肽转移酶、谷胱甘肽还原酶和谷胱甘肽过氧化物酶活性的降低。结论:铝碳酸镁对幽门结扎和乙醇诱发的大鼠胃粘膜损伤具有保护作用,其作用机制与粘膜保护和抗脂质过氧化作用有关。Background/Aims: To evaluate the protective effect and mechanism of Hydrotalcite(Talcid) against gastric mucosal lesions induced by pylorus ligation and ethanol in rats. Methods: Gastric mucosal lesions were induced by oral administration of absolute ethanol and pylorus ligation. Gastric acid secretion, MDA, PGE,, mucosal blood flow, and activities of some enzymes were determined. Results: Oral administration of Hydrotalcite at the dosage of 500mg/kg reduced significantly the gastric lesions induced by ethanol and pylorus ligation, neutralized gastric acid and inhibited the activities of pepsin. Hydrotalcite could promote mucosal blood flow and secretion of PGE2. In addition, Hydrotalcite could decrease the MDA in gastric mucosa induced by ethanol, and prevent the decrease of quinone reductase, glutathion-S-transferases, glutathion reductase, glutathion peroxidase in gastric mucosa. Conclusions: These results suggest that Hydrotalcite has protective effect against ethanol and pylorus ligation-induced gastric mucosal lesions via mucosal protection and anti-lipid peroxidation.
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