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目的:建立一种稳定有效的小鼠模型,为进一步研究全肠外营养(TPN)相关肠黏膜屏障损伤的机制和干预措施。方法:将22只小鼠随机分为对照组(n=10)和TPN组(n=12)。小鼠经颈内静脉置管后,对照组给予正常饮食,用微量泵持续输注等渗盐水;TPN组给予禁食后用微量泵持续输注PN液。5 d后比较两组小鼠生存率、肠道菌群易位情况、肠道杯状细胞数量以及潘氏细胞变化。结果:两组小鼠的生存率无显著性差异。TPN组肠道菌群淋巴结易位率增加(6/10 vs 1/10,P<0.05),杯状细胞数量减少[(61.6±6.5)个vs(33.0±7.8)个,P<0.01)],隐窝处潘氏细胞内抗菌多肽颗粒明显减少,溶菌酶和黏蛋白2(MUC2)含量显著降低。结论:TPN组小鼠能作为后期研究TPN诱导肠黏膜免疫屏障受损的模型,用于患病机制、药物治疗的观察和研究。
OBJECTIVE: To establish a stable and effective mouse model to further investigate the mechanisms and interventions of intestinal mucosal barrier injury associated with total parenteral nutrition (TPN). Methods: Twenty-two mice were randomly divided into control group (n = 10) and TPN group (n = 12). After the mice were placed in the jugular vein, the control group were given normal diet, and the infusion of isotonic saline was continued with the micropump. The TPN group was given continuous infusion of PN fluid with a small amount of pump after fasting. After 5 days, the survival rate, intestinal microflora translocation, intestinal goblet cells and Paneth cells in two groups were compared. Results: There was no significant difference in survival between the two groups of mice. The numbers of goblet cells in the TPN group increased (6/10 vs 1/10, P <0.05), and the number of goblet cells decreased (61.6 ± 6.5 vs 33.0 ± 7.8, P <0.01) , The antibacterial polypeptide particles in the Pampanitsa cells were significantly reduced, and the contents of lysozyme and mucin 2 (MUC2) were significantly decreased. Conclusion: TPN mice can be used as a model for the later study of TPN-induced damage of intestinal mucosal immune barrier for the observation and study of the pathogenesis and drug therapy.