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硫酸化昆布多糖抑制巨噬细胞泡沫细胞的形成。

Sulfated Laminaria japonica polysaccharides inhibit macrophage foam cell formation.

机构信息

School of Food Science and Engineering, Hefei University of Technology, Hefei 230009, People's Republic of China.

School of Food Science and Engineering, Hefei University of Technology, Hefei 230009, People's Republic of China; School of Biological and Medical Engineering, Hefei University of Technology, Hefei 230009, People's Republic of China.

出版信息

Int J Biol Macromol. 2018 May;111:857-861. doi: 10.1016/j.ijbiomac.2018.01.103. Epub 2018 Feb 19.

DOI:10.1016/j.ijbiomac.2018.01.103
PMID:29355629
Abstract

In this work, a purified Laminaria japonica polysaccharide (LJP61A) was chemically modified to obtain three sulfated polysaccharides (SLJP1, SLJP2 and SLJP3) with different degrees of sulfation using the method of chlorosulfonic acid/pyridine. The effects and underlying mechanism of SLJP1, SLJP2 and SLJP3 on the suppression of macrophage foam cell formation were further investigated using the model of oxidized low-density lipoprotein (ox-LDL)-induced foam cell formation. Results exhibited that the macrophage foam cell formation induced by ox-LDL could be significantly alleviated by these sulfated polysaccharides in a dose-dependent manner. Meanwhile, the enhancement of PPAR-γ mRNA expression in ox-LDL induced macrophages was remarkably inhibited by these sulfated polysaccharides. Moreover, the cellular inflammation induced by ox-LDL could also be remarkably mitigated by these sulfated polysaccharides. These results indicated that the sulfated L. japonica polysaccharides could inhibit the conversion of macrophage into foam cell via obstructing PPAR-γ activation and alleviating cellular inflammation.

摘要

在这项工作中,使用氯磺酸/吡啶法对纯化的海带多糖(LJP61A)进行化学修饰,得到了三种不同硫酸化程度的硫酸化多糖(SLJP1、SLJP2 和 SLJP3)。采用氧化型低密度脂蛋白(ox-LDL)诱导泡沫细胞形成模型,进一步研究了 SLJP1、SLJP2 和 SLJP3 对抑制巨噬细胞泡沫细胞形成的作用及作用机制。结果表明,这些硫酸化多糖能剂量依赖性显著减轻 ox-LDL 诱导的巨噬细胞泡沫细胞形成。同时,这些硫酸化多糖显著抑制 ox-LDL 诱导的巨噬细胞中 PPAR-γmRNA 表达的增强。此外,这些硫酸化多糖还能显著减轻 ox-LDL 引起的细胞炎症。这些结果表明,硫酸化海带多糖可通过阻断 PPAR-γ 激活和减轻细胞炎症来抑制巨噬细胞向泡沫细胞的转化。

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