MNNG综合法诱导大鼠胃癌形成的胃组织学与超微结构研究

Study on Gastric Histology and Ultrastructure during the Formation of Gastric Cancer in Rats Induced by MNNG Integrated Method

[目的]探讨N-甲基-N'-硝基-N-亚硝基胍(MNNG)综合法诱导大鼠胃癌(GC)形成过程中胃组织病理学形态与超微结构的变化。[方法]将36只SPF级雄性SD大鼠随机分为正常组与模型组各18只,正常组予常规自由饮食,模型组自由饮用170μg/ml MNNG溶液,喂食含0.03%雷尼替丁饲料,灌服2%水杨酸钠溶液配合饥饱失常法复制GC大鼠模型,于造模后20、24、28、32、48周观察两组大鼠的胃黏膜病理学形态与超微结构的变化。[结果]随着造模时间的增加,模型组大鼠在造模第24周出现肠上皮化生,32周出现异型增生,48周癌变。[结论]MNNG综合法诱导下大鼠胃黏膜肠上皮化生和异型增生向癌症转变可能发生在造模第32~48周,与胃黏膜上皮细胞结构异常有关。

[Objective]To explore the changes of histopathological morphology and ultrastructure of gastric tissue during the formation of gastric cancer in rats induced by N-methyl-N'-nitro-N-nitrosoguanidine(MNNG)integrated method.[Methods]Thirty-six SPF male SD rats were randomly divided into normal group and model group with 18 rats in each group.The normal group was given a conventional free diet,and the model group was given 170μg/ml MNNG solution,0.03%ranitidine,and 2%sodium salicylate solution combined with the irregular diet method to create GC rat model.The pathological morphology and ultrastructure of gastric mucosa were observed at the 20th,24th,28th,32nd and 48th weeks after modeling.[Results]With the increase of the modeling time,rats in the model group developed intestinal metaplasia at the 24th week of the modeling,dysplasia at the 32nd week,and cancer at the 48th week.[Conclusion]The transition from intestinal metaplasia and dysplasia of gastric mucosa to cancer induced MNNG integrated method may occur between the 32nd and 48th week of modeling,which is related to the abnormal structure of gastric mucosal epithelial cells.