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罗氏海盘车多糖在巨噬细胞和环磷酰胺诱导的免疫抑制小鼠模型中的免疫增强作用。

The immunoenhancement effects of starfish Asterias rollestoni polysaccharides in macrophages and cyclophosphamide-induced immunosuppression mouse models.

作者信息

Liu Yingjuan, Wu Xiaolin, Wang Yue, Jin Weihua, Guo Yunliang

机构信息

Institute of Cerebrovascular Diseases, The Affiliated Hospital of Qingdao University, Qingdao 266003, China.

出版信息

Food Funct. 2020 Dec 1;11(12):10700-10708. doi: 10.1039/d0fo01488e. Epub 2020 Nov 21.

Abstract

The water-soluble polysaccharide, SF-2, obtained from starfish (Asterias rollestoni), belongs to the group of polysaccharides known as mannoglucan sulfate. It is composed of mannose as well as glucose and contains 13.85% SO. We aimed to detect the immunoenhancement effects of SF-2 in macrophages and cyclophosphamide (CYP)-induced immunosuppression mouse models. RAW 264.7 macrophage cells were treated with SF-2 for different periods of time (0 h, 0.5 h, 1 h, 3 h, 6 h, and 9 h) and the results showed that SF-2 promoted the production of nitric oxide and up-regulated the levels of pro-inflammatory cytokines and related proteins, such as TNF-α, IL-1β, IL-6, COX-2, MMP-9, and iNOS in a time-dependent manner. In addition, SF-2 activated NLRP3 inflammasome and the MAPK/NF-κB signaling pathway, thus promoting its immunoenhancement effects. Moreover, we co-cultured the primary peritoneal macrophages with SF-2 for 6 h and found that SF-2 enhanced the expression of NLRP3 inflammasome and the release of cytokines. Furthermore, SF-2 significantly increased the body weight, spleen index, thymus index, and inflammatory cell counts in CYP-induced immunosuppression mouse models. These results indicate that SF-2 is a potential immunoenhancement mediator that acts by activating the NLRP3 inflammasome and MAPK/NF-κB pathway.

摘要

从海星(罗氏海盘车)中提取的水溶性多糖SF-2属于硫酸甘露葡聚糖多糖组。它由甘露糖以及葡萄糖组成,含有13.85%的硫酸根。我们旨在检测SF-2在巨噬细胞和环磷酰胺(CYP)诱导的免疫抑制小鼠模型中的免疫增强作用。用SF-2处理RAW 264.7巨噬细胞不同时间段(0小时、0.5小时、1小时、3小时、6小时和9小时),结果表明SF-2以时间依赖性方式促进一氧化氮的产生,并上调促炎细胞因子和相关蛋白的水平,如TNF-α、IL-1β、IL-6、COX-2、MMP-9和iNOS。此外,SF-2激活NLRP3炎性小体和MAPK/NF-κB信号通路,从而促进其免疫增强作用。此外,我们将原代腹腔巨噬细胞与SF-2共培养6小时,发现SF-2增强了NLRP3炎性小体的表达和细胞因子的释放。此外,SF-2显著增加了CYP诱导的免疫抑制小鼠模型的体重、脾脏指数、胸腺指数和炎性细胞计数。这些结果表明,SF-2是一种潜在的免疫增强介质,通过激活NLRP3炎性小体和MAPK/NF-κB途径发挥作用。

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