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为探讨非甾体抗炎药(Non-steroid anti-inflammation drugs,NSAIDs)所致胃粘膜病变的发生机制,本文以大鼠为动物模型,用炎痛喜康灌胃7天后,对胃粘膜主要防御因子和损伤因子进行了测定.结果表明,口服炎痛喜康后胃粘膜前列腺素E_2(PGE_2)含量、血栓素B_2(TXB_2)含量、胃壁结合粘液量(GAM)明显低于正常大鼠(P<0.001).而胃液pH值、胃酸分泌量和胃蛋白酶活性与正常对照组比较无明显差异(均为P>0.05).提示非甾体抗炎药所致胃粘膜病变是由于前列腺素E_2合成减少,致粘液分泌减少,胃粘膜保护因素削弱,同时血栓素B_2合成减少,致血小板不易聚集所致.
In order to explore the pathogenesis of gastric mucosal lesions caused by non-steroid anti-inflammatory drugs (NSAIDs), we used the rat as animal model, Defense factor and injury factor were measured.The results showed that the content of prostaglandin E_2 (PGE_2), TXB2 and gastric mucosa (GAM) in gastric mucosa were significantly lower than those in normal rats P <0.001), while gastric juice pH value, gastric acid secretion and pepsin activity had no significant difference compared with the normal control group (all P> 0.05), suggesting that NSAID-induced gastric mucosal lesions were caused by prostaglandin E2 Synthesis decreased, mucus secretion decreased, gastric mucosal protection factors weakened, while thromboxane B 2 synthesis reduced, resulting in platelet aggregation is not easy.