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目的研究反流性食管炎(RE)基本病机及食管康治疗RE的作用机理。方法将60只雄性Wistar大鼠随机分成假手术组、模型组、食管康组、中成药组(三九胃泰颗粒)、西药组(兰索拉唑+莫沙必利)。采用“4.2mm幽门夹+胃底2/3结扎术”制备反流性食管炎动物模型。相应实验处理后,观察食管下段黏膜病理组织学变化及大鼠食管黏膜组织SOD和GSH含量的表达情况。结果与假手术组相比,模型组大鼠体重明显减轻(P<0.05),食管黏膜肉眼及镜下病理改善明显,评分增高(P<0.05);食管黏膜组织SOD、GSH含量显著降低(P<0.05);与模型组及中成药组相比,食管康组死亡率明显降低(P<0.05),肉眼及病理评分显著降低(P<0.05);与西药组相比,大鼠食管黏膜SOD、GSH含量明显改善(P<0.05)。结论食管康能够明显提高RE大鼠食管黏膜SOD、GSH含量,从而促进食管黏膜损伤修复,改善RE症状。
Objective To study the basic pathogenesis of reflux esophagitis (RE) and the mechanism of esophageal health treatment of RE. Methods Sixty male Wistar rats were randomly divided into sham-operation group, model group, esophageal healthy group, Chinese patent medicine group (Sanjiuweitai granule) and western medicine group (lansoprazole + mosapride). Using “4.2mm pyloric folder + 2/3 gastric fundus ligation” preparation of reflux esophagitis animal model. After the corresponding experimental treatment, the pathological changes of the lower esophageal mucosa and the expression of SOD and GSH in the esophageal mucosa were observed. Results Compared with the sham-operation group, the body weight of the model group was significantly reduced (P <0.05), the pathological changes of the esophageal mucosa under the microscope and the microscope were improved significantly (P <0.05), while the contents of SOD and GSH in the esophageal mucosa were significantly decreased <0.05). Compared with the model group and proprietary Chinese medicine group, the mortality of esophageal group was significantly lower (P <0.05) and the macroscopic and pathological scores were significantly lower (P <0.05). Compared with the western medicine group, the esophageal mucosal SOD , GSH content was significantly improved (P <0.05). Conclusion Esophageal can significantly increase the content of SOD and GSH in esophageal mucosa of RE rats, and promote esophageal mucosal injury repair and improve the symptoms of RE.