IL-15 mutant/Fcγ2a融合蛋白对溃疡性结肠炎模型小鼠的治疗作用及其机制研究

被引:3
作者
陈尧 [1 ]
蒋小华 [2 ,3 ]
郑萍 [4 ]
陶庆松 [3 ]
机构
[1] 东南大学医学院
[2] 同济大学附属东方医院胃肠外科
[3] 东南大学附属中大医院普通外科
[4] 同济大学附属东方医院消化内科
关键词
融合蛋白; 模型溃疡性结肠炎; 白细胞介素15; 小鼠;
D O I
暂无
中图分类号
R574.62 [结肠疾病]; R-332 [医用实验动物学];
学科分类号
100201 [内科学]; 100402 [劳动卫生与环境卫生学];
摘要
目的:探讨IL-15 mutant/Fcγ2a融合蛋白(IL-15 mutant/Fc)对溃疡性结肠炎(UC)小鼠模型的治疗作用及其可能的作用机制。方法:5%葡聚糖硫酸钠(DSS)连续饮用制成UC模型,随机将30只小鼠分为对照组、IL-15 mutant/Fc治疗组、Ig G2a治疗组,观察小鼠一般体重情况。造模完成后取结肠行大体病理观察,并行伊红染色,查看其病理学损伤水平。ELISA分析小鼠眼球血的IL-10、IL-15、TNF-α炎症因子的含量,RT-PCR测定结肠组织STAT3和STAT5 mRNA的表达,蛋白质印迹法测定磷酸化STAT5(p-STAT5)以及磷酸化AKT(p-AKT)蛋白的表达。结果:除对照组小鼠外,其他两组均出现一般情况及体重改变。而IL-15mutant/Fc组小鼠的症状以及组织病理学评分均轻于Ig G2a组。IL-15 mutant/Fc可改善IL-10、IL-15、TNF-α的分泌情况。IL-15 mutant/Fc抑制STAT5 mRNA、STAT3 mRNA表达以及p-STAT5、p-AKT蛋白的表达。结论:IL-15 mutant/Fc在体内具有改善模型UC小鼠病情的作用,它可能通过特异性的拮抗IL-15受体来干预STAT、AKT信号通路的信号转导而发挥其治疗作用。
引用
收藏
页码:559 / 564
页数:6
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