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目的评价慢性萎缩性胃炎N-甲基-N’-硝基-N-亚硝基胍(MNNG)复合造模法的稳定性及对动物肝脏的影响。方法 60只SPF级健康雄性SD大鼠随机分为正常组8只及造模1组、造模2组各26只。造模1组用MNNG复合高盐热淀粉糊法、造模2组采用MNNG复合乙醇灌胃法制备慢性萎缩性胃炎大鼠模型,正常组正常饲养。造模时间28周。造模后比较造模1组、造模2组大鼠胃黏膜病理程度,血清胃蛋白酶原Ⅰ(PGⅠ)、胃蛋白酶原Ⅱ(PGⅡ)及肝脏病理改变。结果造模1组大鼠24周出现腺体异型增生,26周出现灶性肠化生。造模2组大鼠26周出现个别腺体异型增生,28周出现灶性肠化生。模型1组死亡率为26.9%,模型2组为15.4%。造模后造模1组、造模2组大鼠胃黏膜病理改变差异无统计学意义(P>0.05)。与正常组比较,造模1组、造模2组血清PGⅠ、PGⅠ/PGⅡ降低(P<0.05)。28周造模1组及造模2组大鼠肝脏细胞均出现水样变性。结论慢性萎缩性胃炎MNNG复合造模法造模时间较长,模型死亡率较高,并且对大鼠肝脏组织有一定影响。
Objective To evaluate the stability of animal model of chronic atrophic gastritis combined with N-methyl-N’-nitro-N-nitrosoguanidine (MNNG) and its effect on animal liver. Methods Sixty SPF healthy male SD rats were randomly divided into normal group (n = 8), model group (n = 1) and model group (n = 26). The rats in model group were treated with MNNG complex high-salt hot starch paste method, and the rats in model group were treated with MNNG complex ethanol gavage to establish chronic atrophic gastritis rat model. The rats in normal group were reared normally. Modeling time of 28 weeks. After modeling, the pathological changes of gastric mucosa, PGⅠ, PGⅡ and pathological changes of liver in model group 1 were made. Results The rats in model group had glandular dysplasia at 24 weeks and focal intestinal metaplasia at 26 weeks. There were some gonad dysplasia at 26 weeks in model 2 rats and focal intestinal metaplasia at 28 weeks. The mortality of model 1 group was 26.9% and that of model 2 group was 15.4%. There were no significant differences in the pathological changes of gastric mucosa between model group 1 and model group 2 (P> 0.05). Compared with normal group, the levels of PGⅠ and PGⅠ / PGⅡ in model group 1 and model group 2 were decreased (P <0.05). 28 weeks model group 1 and model 2 rat liver cells were watery degeneration. Conclusions Chronic atrophic gastritis (MNNG) model has a longer duration of modeling, higher mortality and a certain influence on rat liver tissue.