脾胃虚寒型胃溃疡病证结合大鼠实验模型的建立及评价研究

目的:建立脾胃虚寒型胃溃疡(GU)病证结合大鼠实验模型并对其进行客观评价。方法:36只SD大鼠按随机数字方法分为正常组、模型组和黄芪建中汤组(HQJZT)3组,采用“苦寒泻下+劳倦过度”法联合“乙醇+阿司匹林”造模,观察大鼠的一般症状与体征,测定体质量、进食量、饮水量、肛温,计算溃疡指数,HE染色观察黏形态学改变,ELISA法测定NO、MDA、PGE含量,免疫组化检测TLR-2、MyD88蛋白表达。结果:与正常组比较,模型大鼠体质量、进食量、肛温均显著降低,总体或局部症状与体征、胃黏膜形态均发生病性改变。给予HQJZT后上述指标均明显提高或明显改善,与正常组比较,模型大鼠胃黏膜PGE、NO含量显著降低,MDA含量明显增加,TLR-2、MyD88蛋白表达明显上调;给予HQJZT后PGE、NO含量显著增加,MDA含量明显降低,TLR-2、MyD88蛋白表达显著下调,与模型组比较差异有统计学意义。结论:本研究构建了可靠、稳定的脾胃虚寒型GU病证结合大鼠实验模型,该模型可为中医药防治GU的临床研究奠定基础。

Establishment and Evaluation of the Combination of Disease And Syndrome Experimental Model of Spleen Stomaeh Deficieney Cold Type of Gastric Ulcer in Rats

Objective:To establish and evaluate an experimental model of gastric ulcer(GU)in rats with syndrome of spleen-stomach deficiency cold and to evaluate it objectively.Methods:SD rats were randomly divided into normal group,model group,and Huang-Qi-Jian-Zhong-Tang(HQJZT)group.The animal model was established by using method of"bitter cold induced diarrhea+overfatigue"combined with"ethanol+aspirin".The general symptoms and signs of the rats were observed.Body weight,food intake,water intake,and rectal temperature were measured.The degree of mucosal damage was observed and the ulcer index was calculated.The pathological changes of mucous membrane were observed by HE staining.The contents of No,MDA,and PGE were detected by ELISA.The expression of TLR-2 and MyD88 protein were detected by immunohistochemistry.Results:The body weight,food intake,and rectal temperature of the model group were significantly reduced when compared with the normal group.The general or local symptoms and signs and the gastric mucosa were significantly changed,however,the above indicators were significantly increased or improved after the administration of HQJZT.The contents of PGE and NO in gastric mucosa of model group were significantly decreased,the content of MDA was significantly increased,and the expression of TLR-2 and MyD88 protein were significantly upregulated when compared with the normal group.In contrast,the contents of PGE and NO were significantly increased,the content of MDA was significantly decreased,and the expression of TLR-2 and MyD88 protein were significantly decreased after the administration of HQJZT,when compared with the ulcer model group.Conclusion:The experimental model of GU in rats with syndrome of spleen-stomach deficiency cold was established successfully in this study.The model was stable,reliable,and reproducible,which could lay a foundation for clinical research of traditional Chinese medicine in the prevention and treatment of GU.