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Molecular mechanism of a new Laminaria japonica polysaccharide on the suppression of macrophage foam cell formation via regulating cellular lipid metabolism and suppressing cellular inflammation
Author(s) -
Zha XueQiang,
Xue Lei,
Zhang HaiLin,
Asghar MuhammadNaeem,
Pan LiHua,
Liu Jian,
Luo JianPing
Publication year - 2015
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201500113
Subject(s) - foam cell , cd36 , scavenger receptor , lipid metabolism , inflammation , chemistry , biochemistry , receptor , microbiology and biotechnology , macrophage , cholesterol , biology , lipoprotein , immunology , in vitro
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 μg/mL LJP61A. Meanwhile, LJP61A caused a remarkable decrease in mRNA expression of peroxisome proliferator‐activated receptor γ 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)‐α‐ d ‐Man p‐ (1→, →4)‐α‐ d ‐Man p‐ (1→, →4)‐2‐ O ‐acetyl‐β‐ d ‐Glc p ‐(1→, →4)‐β‐ d ‐Glc p‐ (1→, →6)‐4‐ O ‐SO 3 ‐β‐ d ‐Gal p‐ (1→, →6)‐β‐ d ‐Gal p‐ (1→, →3)‐β‐ d ‐Gal p‐ (1→, and a terminal residue of α ‐ d ‐ Glc p‐ (1→. Conclusion Our findings suggest that LJP61A inhibits the conversion of macrophage into foam cell via regulating cellular lipid metabolism and suppressing cellular inflammation.