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Dilinoleoylphosphatidylcholine induces the expression of the anti‐inflammatory heme oxygenase‐1 in RAW264.7 macrophages
Author(s) -
Son Yong,
Lee Ju Hwan,
Kim NamHo,
Surh NaYoung,
Kim EunCheol,
Chung HunTaeg,
Kang Dae Gill,
Pae HyunOck
Publication year - 2010
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.87
Subject(s) - proinflammatory cytokine , heme oxygenase , chemistry , tumor necrosis factor alpha , heme , nitric oxide synthase , lipopolysaccharide , copp , nitric oxide , inflammation , pharmacology , biochemistry , enzyme , biology , immunology , organic chemistry
1,2‐Dilinoleoyl‐ sn ‐glycero‐3‐phosphocholine (DLPC), the main and active component of soybean lecithin, has been reported to exert anti‐inflammatory effects, but the underlying mechanisms remain to be established. It was found that DLPC could induce the expression of the anti‐inflammatory heme oxygenase‐1 (HO‐1) through the activation of nuclear erythroid 2‐related factor 2 (Nrf2) in RAW264.7 macrophages. Pretreatment with DLPC suppressed the expression of inducible nitric oxide (NO) synthase (iNOS), one of proinflammatory enzymes, and reduced NO production in lipopolysaccharide (LPS)‐stimulated macrophages. Similarly, DLPC also diminished the production of tumor necrosis factor‐α (TNF‐α), one of proinflammatory cytokines. Interestingly, the inhibitory effects of DLPC on LPS‐induced iNOS expression and TNF‐α production were reversed by tin protoporphyrin, a HO‐1 inhibitor. Thus, HO‐1 expression via Nrf2 activation may be one of the possible mechanisms explaining the anti‐inflammatory effects of DLPC.