建立萎缩性胃炎伴异型增生大鼠脾胃气虚、毒损胃络病证结合模型的探索

Exploration on Establishing Animal Model of Chronic Atrophic Gastritis Combined with Spleen- stomach Deficiency and Toxin Damage to Stomach Vessels

目的建立慢性萎缩性胃炎伴异型增生大鼠脾胃气虚、毒损胃络病证结合的实验模型。方法以120μg/ml的N-甲基-N'-硝基-N-亚硝基胍(MNNG)溶液灌胃为基础,配合自由饮用浓度为0.05%氨水溶液,进食含0.03%盐酸雷尼替丁大鼠饲料,进行造模。于实验第20周起每4周分别随机抽检2只,检测模型复制程度。记录大鼠宏观表征、体质量、饮水、进食量。造模成功后,停止干预12周,观察自然恢复组胃黏膜病理变化情况。结果于第32周成功建立异型增生大鼠模型,且模型组表现出偏小,皮毛散乱,黯淡无光,蜷缩少动喜扎堆,尾部紫暗,舌质瘀紫等表征,体重、饮水量、进食量均低于正常组。停止干预12周后自然恢复组胃黏膜病理仍为异型增生表现。结论采用MNNG灌胃,配合低浓度氨水、雷尼替丁喂养,所建立的萎缩性胃炎合并异型增生大鼠模型,符合脾胃气虚、毒损胃络的中医证候表现,模型较为稳定。

Objective To establish the animal model of chronic atrophic gastritis combined with spleen- stomach deficiency and toxin damage to stomach vessels. Methods In 120 g / ml N- methyl- N’- nitro- N- nitrosoguanidine( MNNG) by gavage based solution,rats were given 5ml / kg / day,with free drinking concentration of 0. 05% ammonia solution,as well as food containing 0. 03% ranitidine hydrochloride,thus the models were established. Starting from the twentieth week,two rats were randomly chose for every 4 weeks to detect molding degree. Characterization of rats,body weight,food and water intake were recorded. After the successful modeling,intervention was stopped for 12 weeks to observe gastric mucosa pathological changes of natural restoration. Results The animal model was successfully established on the 32 thweek,and the rats showed small shape,scattered bleak fur,curled up hair,few motions,gathered together,dark purple in tail,purple tongue with stasis characterization,lower weight,lower water and food intake compared with normal group. Twelve weeks after intervention,natural recovery group of gastric mucosal pathology still showed dysplasia. Conclusion MNNG gavage,with low concentration of ammonia,ranitidine feeding to build rat models of atrophic gastritis with dysplasia is consistent with the TCM syndrome manifestations of qi deficiency of spleen and stomach,stomach meridian poison damage,and the model is stable.