首页> 中文期刊> 《中国实验动物学报》 >不同浓度葡聚糖硫酸钠对小鼠炎症性肠病模型建立及其致病相关免疫因子表达的影响

不同浓度葡聚糖硫酸钠对小鼠炎症性肠病模型建立及其致病相关免疫因子表达的影响

             

摘要

目的:探讨饮用不同浓度的葡聚糖硫酸钠( dextran sulfate sodium, DSS)对于建立小鼠炎症性肠病( inflammatory bowel disease, IBD)模型及其致病相关免疫因子表达的影响。方法雄性C57BL/6J小鼠随机分为对照组和不同浓度的DSS饮用组(3%、5%、7%)。观察小鼠的大便性状,体重和生存时间。饮用后的第6天处死各组小鼠,观察结肠大体形态并评分;取病变处进行石蜡包埋病理切片,苏木素伊红染色并进行病理组织学评分;定量PCR检测各组脾细胞免疫因子表达情况。结果饮用3%、5%、7%浓度DSS的小鼠在第6天均有不同程度溃疡形成,成模率随着DSS浓度提升而增加,但是小鼠死亡率也相应增加。定量PCR结果表明促炎因子( TNF-α、IFN-γ和IL-17A)的表达水平与DSS浓度成正相关,而抑炎因子( IL-4和IL-10)以及调节性T细胞相关的转录因子Foxp3的表达水平与DSS浓度成负相关关系。结论给予小鼠5%浓度的DSS溶液饮用有助于高效经济地建立小鼠IBD模型,为进一步研究IBD的发病机理、生物学特性、干预因素等打下了重要基础。%Objective The aim of this study was to investigate how different concentrations of dextran sulfate sodi-um ( DSS) influence the establishment of mouse model of inflammatory bowel disease ( IBD) and the effect of DSS on the expression of colitis-associated immune factors.Methods The DSS solution in different concentrations (3%, 5%, 7%) were given to male C57BL/6J mice to generate mouse inflammatory bowel disease model.The IBD mice were observed by defecation characteristics, body weight, and survival time.The animals were sacrificed at 6 days after the start of DSS drinking.The general appearance of colons was observed and scored.Moreover, the pathological changes of the colon were examined and analyzed by routine histology.The expression of immune factors in the spleen was detected by real-time PCR.Results The mice in the 3%, 5%, 7% DSS groups developed murine colitis.In addition, the incidence of IBD and mouse mortality rate was directly proportional to the increase of DSS concentration.Furthermore, the higher concentra-tion of DSS induced the expression of proinflammatory factors including TNF-α, IFN-γand IL-17A, but cause a decrease of anti-inflammatory factors such as IL-4, IL-10 and Treg-related transcription factor Foxp3.Conclusions Our data suggest that giving 5%DSS solution to C57BL/6J mouse is appropriate to efficiently establish a murine IBD model.This laid an important foundation for further studies of the pathogenesis of IBD, biological characteristics, and intervention factors.

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