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壳寡糖激活巨噬细胞的机制

2022-07-13 09:16:03

摘要: 目的:探讨巨噬细胞结合、内吞壳寡糖以及壳寡糖激活巨噬细胞的机制。


方法:利用荧光物质2-氨基吖啶酮标记壳寡糖,在激光共聚焦显微镜下观察巨噬细胞内吞壳寡糖的过程,流式细胞仪分析细胞的荧光强度,通过竞争性抑制实验及钙离子、胰蛋白酶、秋水仙碱对内吞的影响来确定巨噬细胞内吞壳寡糖的机制.通过RT-PCR方法检测TNF-α来反映结合及内吞过程对壳寡糖刺激巨噬细胞的影响。


结果:巨噬细胞可结合内吞壳寡糖。内吞易受温度影响,37℃较迅速(<2 min),4℃只能结合不能内吞。EDTA可抑制巨噬细胞内吞壳寡糖;经胰蛋白酶预处理的巨噬细胞摄取壳寡糖的能力大大降低,终止胰蛋白酶后巨噬细胞摄取壳寡糖的能力得到恢复。秋水仙碱预处理可明显抑制巨噬细胞摄取壳寡糖,并呈剂量依赖性。0.1 mol/L甘露糖可抑制壳寡糖对巨噬细胞的刺激作用。


结论:甘露糖受体介导的吞饮是巨噬细胞内吞壳寡糖的一条重要途径,甘露糖受体在壳寡糖激活巨噬细胞中起重要作用。


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