黑灵芝多糖对脂多糖诱导巨噬细胞M1/M2表型转化的影响

doi:10.7506/spkx1002-6630-201819022

食品科学 ›› 2018, Vol. 39 ›› Issue (19): 141-146.doi: 10.7506/spkx1002-6630-201819022

黑灵芝多糖对脂多糖诱导巨噬细胞M1/M2表型转化的影响

刘想1，付王威2，牛晓琴2，颜雨新1，张贤益2，李文娟2,*

1.南昌大学医学院，江西南昌 330008；2.南昌大学食品科学与技术国家重点实验室，江西南昌 330047

出版日期:2018-10-15 发布日期:2018-10-24
基金资助:
国家自然科学基金地区科学基金项目（31560460）；江西省科技厅自然科学基金项目（20151512041185）；食品科学与技术国家重点实验室青年研究基金项目（SKLF-QN-201509）

Effect of Ganoderma atrum Polysaccharide on M1/M2 Polarization in Lipopolysaccharide (LPS)-Stimulated Macrophages

LIU Xiang1, FU Wangwei2, NIU Xiaoqin2, YAN Yuxin1, ZHANG Xianyi2, LI Wenjuan2,*

1. Medical College, Nanchang University, Nanchang 330008, China; 2. State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, China

Online:2018-10-15 Published:2018-10-24

摘要/Abstract

摘要： 目的：观察黑灵芝多糖对脂多糖（lipopolysaccharide，LPS）诱导小鼠腹腔巨噬细胞M1/M2表型转化的影响。方法：中性红检测巨噬细胞吞噬；流式细胞仪检测细胞活性氧（reactive oxygen species，ROS）和甘露糖受体（mannose receptor，MR）水平；Griess法测定NO水平；酶联免疫吸附实验测定细胞因子白细胞介素（interleukin， IL）-1β和IL-10水平。结果：与LPS组相比，黑灵芝多糖可显著降低巨噬细胞吞噬能力并抑制IL-1β、NO和ROS的生成，提示黑灵芝多糖可抑制巨噬细胞向M1表型极化。同时，黑灵芝多糖可上调LPS处理的巨噬细胞MR表达和IL-10 水平，促进巨噬细胞向M2表型极化。在黑灵芝多糖＋LPS组中加入MR抑制剂，发现黑灵芝多糖抗LPS介导的炎症反应有所减弱。结论：黑灵芝多糖对LPS致炎巨噬细胞极化表型具有调控作用，且其可通过MR抑制巨噬细胞向M1 表型极化而促进向M2表型极化。

关键词: 黑灵芝多糖, 巨噬细胞极化, 甘露糖受体, 调控作用, 炎症反应

Abstract: Objective: The aim of this study was to explore the regulatory effect of Ganoderma atrum polysaccharide (PSG-1) on M1/M2 polarization in lipopolysaccharide (LPS)-simulated mouse macrophages. Methods: Neutral red assay was used to detect macrophage phagocytosis, and flow cytometry analysis was used to determine the level of reactive oxygen species (ROS) and the expression of mannose receptor (MR). Nitric oxide (NO) was analyzed by the Griess method and the levels of interleukin-1β (IL-1β) and IL-10 were determined by enzyme-linked immunosorbent assay (ELISA). Results: Compared to the LPS group, PSG-1 could remarkably reduce macrophage phagocytosis, and inhibit the secretion of IL-1β and NO, but down-regulate the generation of ROS, suggesting that PSG-1 could inhibit LPS-caused macrophage polarization into M1. Meanwhile, significant elevations of MR expression and IL-10 level were observed in the PSG-1 + LPS group compared to LPS group, indicating that PSG-1 promoted macrophage polarization into M2. Further results showed that the inhibitory effect of PSG-1 against LPS-induced inflammatory response was decreased evidently in macrophages by the treatment of anti-MR antibody. Conclusion: PSG-1 has a distinct regulatory effect on LPS-mediated macrophage polarization via inhibiting polarization into M1 and enhancing polarization into M2. Its molecular mechanism may be closely related to the regulation of MR expression on the surface of macrophages.

Key words: Ganoderma atrum polysaccharide, macrophage polarization, mannose receptor, regulatory effect, inflammatory response

中图分类号:

TS201.4

刘想，付王威，牛晓琴，颜雨新，张贤益，李文娟. 黑灵芝多糖对脂多糖诱导巨噬细胞M1/M2表型转化的影响[J]. 食品科学, 2018, 39(19): 141-146.

LIU Xiang, FU Wangwei, NIU Xiaoqin, YAN Yuxin, ZHANG Xianyi, LI Wenjuan. Effect of Ganoderma atrum Polysaccharide on M1/M2 Polarization in Lipopolysaccharide (LPS)-Stimulated Macrophages[J]. FOOD SCIENCE, 2018, 39(19): 141-146.

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黑灵芝多糖对脂多糖诱导巨噬细胞M1/M2表型转化的影响

Effect of Ganoderma atrum Polysaccharide on M1/M2 Polarization in Lipopolysaccharide (LPS)-Stimulated Macrophages

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