目的 探究黄芪多糖-Ⅱ（Astragalus polysaccharides-Ⅱ，APS-Ⅱ）在微褶皱细胞上的转运机制。方法 通过人结直肠腺癌Caco-2细胞和人Burkitt淋巴瘤Raji细胞共培养构建微褶皱细胞模型；将APS-Ⅱ进行荧光标记，分别加入Toll样受体4（Toll-like receptor 4，TLR4）、TLR2、C型凝集素-1（dendritic cell-associated C-type lectin-1，Dectin-1）和补体成分5a受体（complement component 5a receptor 1，C5aR）抑制剂，以探讨各受体在APS-Ⅱ转运中的作用。结果 TLR4受体抑制剂和C5aR受体抑制剂显著减少了APS-Ⅱ的转运量（P＜0.001），表明APS-Ⅱ的转运可能与TLR4和C5aR受体有关，相反，TLR2受体抑制剂和Dectin-1受体抑制剂未显著影响APS-Ⅱ的转运量，提示TLR2和Dectin-1受体可能不参与APS-Ⅱ的转运。结论 APS-Ⅱ在微褶皱细胞上的转运机制可能依赖于TLR4和C5aR受体，而TLR2和Dectin-1受体可能不参与此过程。

Objective To investigate the transport mechanism of Astragalus polysaccharide-II (APS-II) in microfold cells (M cells). Methods M cells model was constructed using Caco-2 and Raji cells. APS-II was labeled with fluorescence, and Toll-like receptor 4 (TLR4), TLR2, dendritic cell-associated C-type lectin-1 (Dectin-1) and complement component 5a receptor 1 (C5aR) inhibitors were added respectively, to explore the role of each receptor in the transport of APS-II. Results TLR4 and C5aR inhibitors significantly reduced the transport of APS-II, indicating that transport of APS-II may be related to TLR4 and C5aR receptors. In contrast, TLR2 and Dectin-1 inhibitors did not significantly affect transport of APS-II, suggesting that these receptors may not be involved in the transport of APS-II. Conclusion Transport mechanism of APS-II in M cells may depend on TLR4 and C5aR receptors, while TLR2 and Dectin-1 receptors may not be involved in this process.

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国家自然科学基金资助项目（81872962）;国家博士后科学基金资助项目（2019M650851）;国家重点研发计划项目（2019YFC1710山西省重点研发计划重点项目（201603D311101）;山西省优秀人才科技创新项目（201605D211030，201705D211020）;山西省科技创新人才团队专项基金