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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?
OBJECTIVE: To prepare a non-steroidalanti-inflammatory drug (NSAID) -induced gastric mucosal lesion in rats and to study its mechanism of action and prevention of misoprostol (omeprazole, smecta, sucralfate) effect. METHODS: NSAID-induced gastric mucosa injury was induced by aspirin and indomethacin in rats. The damage of NSAID-induced gastric mucosal injury and the morphological changes of gastric mucosa were observed with light microscope and scanning electron microscope. Determination of gastric mucus gel layer thickness, mucosa 6keto PGF1α, TXB2 levels. Results: The injury group caused obvious gastric mucosal lesion with thinning of mucous gel layer, and the decrease of 6-keto-PGF1α and TXB2 in the mucosa (the inhibition rates were 9808% and 9902% respectively). Four kinds of drug prevention and treatment to varying degrees reduce NSAID gastric mucosal damage to misopros tol the most obvious smecta second. Misoprostol significantly increased intramucosal 6 keto PGF1α and TXB2 levels, while increasing the thickness of mucus gel layer. smecta can increase the thickness of mucus gel layer, the degree is weaker than misoprostol, but stronger than sucralfate; omeprazole group mucus layer thickness than the injury group no difference. Scanning electron microscopy and pathological damage index and mucus layer thickness change?