4.7 Article

Hypolipidemic effects of fucoidan fractions from Saccharina sculpera (Laminariales, Phaeophyceae)

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出版社

ELSEVIER
DOI: 10.1016/j.ijbiomac.2019.08.002

关键词

Fucoidan; Saccharina sculpera; Hypolipidemic; Mechanism

资金

  1. National Key Research and Development Program of China [2018YFD0901104]
  2. National Natural Science Foundation of China [31301449, 31471610]
  3. China Agriculture ResearchSystem [CARS-50]

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Fucoidan is a kind of brown algae-derived macromolecule suggested to have hypolipidemic activity. Saccharina sculpera has attracted interest because it is rich in fucoidan. The monosaccharide composition and structural characteristics of isolated fractions (F1, F2 and F3) were determined using high-performance liquid chromatography (HPLC), Fourier transform infrared spectroscopy (FTIR) and nuclear magnetic resonance spectroscopy (NMR). The hypolipidemic effects of fucoidan fractions from Saccharina sculpera cultured in northern China were clarified by measuring cholesterol levels, antioxidative indicators and hepatic gene mRNA expression using an established hyperlipidemic Wistar rat model. The results showed that F1 is an acetylated galactofucan and that F2 consists of fucose, galactose, mannose and glucuronic acid. F3 is an acetylated galactofucan with high fucose. Fucoidan fractions from Saccharina sculpera could effectively reduce the level of lipids in serum by reducing the TG, TC, and LDL-C levels and increasing HDL-C levels and could effectively prevent lipid accumulation in the liver. The findings obtained from hepatic gene expression showed that fucoidan could inhibit cholesterol synthesis via downregulation of HMG-CoA-R and upregulation of LCAT, slow the synthesis of fatty acids via downregulation of SREBP-1c, and promote beta-oxidation of fatty acids via upregulation of PPAR alpha, PPAR gamma and LPL. These results demonstrated that the hypolipidemic activity of fucoidan was related to the inhibition of cholesterol synthesis and reverse transport, the regulation of fatty acid synthesis, and acceleration of mitochondrial beta-oxidation. (C) 2019 Elsevier B.V. All rights reserved.

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