摘要
目的：制备大鼠非甾体类抗炎药（Ｎｏｎ－ｓｔｅｒｏｉｄａｌａｎｔｉ－ｉｎｆｌａｍｍａｔｏｒｙｄｒｕｇｓ，ＮＳＡＩＤ）性胃粘膜损伤动物模型，研究其发生机制及预防应用四种药物（ｍｉｓｏｐｒｏｓｔｏｌ，ｏｍｅｐｒａｚｏｌｅ，ｓｍｅｃｔａ，ｓｕｃｒａｌｆａｔｅ）时的保护作用。方法：联合应用阿斯匹林和消炎痛制备大鼠ＮＳＡＩＤ性胃粘膜损伤模型，用光镜和扫描电镜观察大鼠ＮＳＡＩＤ性胃粘膜损伤及四种药物预防应用时胃粘膜的形态学改变，同时测定胃粘液凝胶层厚度，粘膜６ｋｅｔｏＰＧＦ１α、ＴＸＢ２水平。结果：损伤组引起明显胃粘膜损害，伴粘液凝胶层变薄，粘膜内６ｋｅｔｏＰＧＦ１α和ＴＸＢ２水平下降（抑制率分别为９８０８％和９９０２％）。四种药物预防应用能不同程度减轻ＮＳＡＩＤ性胃粘膜损伤，以ｍｉｓｏｐｒｏｓｔｏｌ最明显，ｓｍｅｃｔａ次之。ｍｉｓｏｐｒｏｓｔｏｌ显著提高粘膜内６ｋｅｔｏＰＧＦ１α和ＴＸＢ２水平，同时增加粘液凝胶层厚度。ｓｍｅｃｔａ可增加粘液凝胶层厚度，程度较ｍｉｓｏｐｒｏｓｔｏｌ弱，而较ｓｕｃｒａｌｆａｔｅ强；ｏｍｅｐｒａｚｏｌｅ组粘液层厚度较损伤组无区别。扫描电镜所见与病理学损伤指数及粘液层厚度改变?
Abstract Aims : To study the mechanism of nonsteroidal antiinflammatory drugs(NSAID,aspirin+indomethacin) induced gastric mucosal damage and the gastroprotective effect of 4 drugs(misoprostol、omeprazole、smecta、sucralfate).Method: NSAID induced gastric mucosal damage model in rats was obtained by pouring mixture of aspirin and indomethacin.Gastric damage was morphologically assessed in the rat stomach by light and scanning electronic microscopy. Thickness of the mucus gel layer adherent to gastric mucosa, gastric mucosal 6-keto PGF 1α 、TXB 2 level were measured as well.Results: NSAID demonstrated evident gastric damage. Light microscopic lesion index wes 2.75±0.46. Surface ultrastructral lesion included extensive cellular exfoliation, some of which with exposure of lamina propiar. A marked reduction in thichness of mucus gel layer, a powerful inhinbition on 6-keto-PGF 1α and TXB 2 level (98.08% adn 99.02% vs control) were detected at the same time. Pretreatment with each of the 4 drugs could reduce mucosal damage in varying extenses. Misoprostol significantly increased mucosal 6-keto-PGF 1α 、TXB a level and raised mucus gel thickness, thus kept the continuity of surface epithelial cells and maintained the most effective protection. Smecta and sucralfate could thicken
出处
《胃肠病学和肝病学杂志》
CAS
1998年第1期20-25,共6页
Chinese Journal of Gastroenterology and Hepatology
