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目的:利用速激肽受体2(tachykinin receptor 2,Tacr2)基因敲除小鼠及诱导溃疡性结肠炎(ulcerative colitis,UC)小鼠模型,探讨Tacr2在小鼠UC发生、发展中的作用。方法 :小鼠按照基因型分成野生型组和基因敲除(纯合子)组,再按照给药与否进一步分成野生型造模组、纯合子造模组、野生型空白组、纯合子空白组。给造模组小鼠口服右旋葡聚糖硫酸钠(dextran sodium sulfate,DSS)构建UC小鼠模型,观察其UC活动指数及结肠组织中病理学改变、炎症因子及上游转录因子核因子NF-κB(nuclear factor-kappa B,NF-κB)的变化。结果:Tacr2基因敲除的纯合子小鼠经DSS诱导的UC症状比野生型造模组小鼠明显加重。进一步分析基础状态下结肠的免疫活性,发现在基础状态下,纯合子小鼠与野生型小鼠相比,结肠免疫活性明显降低,表现为结肠黏膜中IL-1β、TNF-α、IL-6和NF-κB水平降低。结论:Tacr2对UC的发生、发展有抑制作用。
OBJECTIVE: To investigate the role of Tacr2 in the development and progression of mouse UC by using Tacr2 gene knockout mice and inducing ulcerative colitis (UC) mouse models. Methods: Mice were divided into wild-type group and knock-out (homozygous) group according to their genotypes, and then divided into wild type model group, homozygous model group, wild type blank group and homozygous blank group . The mouse model of UC was established by oral administration of dextran sodium sulfate (DSS) to mice in model group. The changes of UC activity index and histopathological changes, inflammatory factors and the expression of NF- κB (nuclear factor-kappa B, NF-κB) changes. Results: The DSS-induced UC symptoms of homozygous Tacr2 knockout mice were significantly worse than those of WT mice. Further analysis of colonic mucosal immunocompetence showed that colonic mucosal immunoreactivity was significantly lower in the basal state compared with wild-type mice, showing a significant decrease of IL-1β, TNF-α, IL-6 And decreased NF-κB levels. Conclusion: Tacr2 has an inhibitory effect on the occurrence and development of UC.