Journal
MOLECULAR NUTRITION & FOOD RESEARCH
Volume 59, Issue 10, Pages 2008-2021Publisher
WILEY
DOI: 10.1002/mnfr.201500113
Keywords
Foam cell; Laminaria japonica; Molecular mechanism; Polysaccharide; Structure
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Funding
- National Natural Science Foundation of China [31271814, 21006019]
- Specialized Research Fund for the Doctoral Program of Higher Education of China [20130111110001]
- Fundamental Research Funds for the Central Universities [2014HFCH0011]
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Scope: Laminaria japonica is an important marine vegetable with great health benefits for preventing atherosclerosis. Since the foam cell formation is an important hallmark for the initiation of atherosclerosis, we examined the effect and underlying mechanism of a purified L. japonica polysaccharide (LJP61A) on the suppression of macrophage foam cell formation in this study. The chemical structure was further characterized. Methods and results: Using oxidized low-density lipoprotein (ox-LDL)-induced foam cell model, we found that the cellular lipid accumulation was significantly attenuated by 25 mu g/mL LJP61A. Meanwhile, LJP61A caused a remarkable decrease in mRNA expression of peroxisome proliferator-activated receptor gamma that was accompanied by the reduction of CD36 and Acyl coenzyme A: cholesterol acyltransferase-1 mRNA levels, and the enhancement of ATP-binding cassette transporters A1 and scavenger receptor B1 mRNA levels. Besides these, the ox-LDL-induced cellular inflammation was also restricted by LJP61A treatment via mammalian target of rapamycin-mediated Toll-like receptor 2/4-Mitogen-activated protein kinases/nuclear factor kappa-B pathways. The structure of LJP61A was characterized as a repeating unit consisting of -> 3,6)-alpha-D-Manp-(1 ->, -> 4)-alpha-D-Manp-(1 ->, -> 4)-2-O-acetyl-beta-D-Glcp-(1 ->, -> 4)-beta-D-Glcp-(1 ->, -> 6)-4-O-SO3-beta-D-Galp-(1 ->, -> 6)-beta-D-Galp-(1 ->, -> 3)-beta-D-Galp-(1 ->, and a terminal residue of alpha-D-Glcp-(1 ->. Conclusion: Our findings suggest that LJP61A inhibits the conversion of macrophage into foam cell via regulating cellular lipid metabolism and suppressing cellular inflammation.
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