title: Effects of soy pinitol on the pro-inflammatory cytokines and scavenger receptors in oxidized low-density lipoprotein-treated THP-1 macrophages.
abstract: Pinitol, a methylated form of D-chiro-inositol, acts as a insulin mediator. We investigated the effects of soy pinitol on the factors involved in foam cell formation using differentiated THP-1 macrophages. Pinitol slightly inhibited the lipid-laden foam cell formation by oxidized low-density lipoprotein (oxLDL) in a dose-dependent manner. Tumor necrosis factor-alpha and monocyte chemoattractant protein-1 releases were significantly reduced by pinitol treatment (0.05-0.5 mM), whereas interleukin-1beta and interleukin-8 secretions were significantly reduced in low-dose pinitol (0.05 or 0.1 mM) and 0.5 mM pinitol-treated cells, respectively, compared to no pinitol-treated cells. Gene expressions of CD36 and CD68 were significantly down-regulated by 0.05-0.5 mM pinitol compared to the oxLDL-treated control cells. Matrix metalloproteinase-9 gene expression was significantly decreased in 0.05-0.5 mM pinitol-treated cells compared to the no pinitol-treated macrophages. We conclude that pinitol has some inhibitory effects on foam cell formation by reducing lipid accumulation, secretion, and expression of some cytokines and macrophage scavenger receptor expression via its insulin-like action.
authors.affiliation: Department of Food Science and Nutrition, Kyungpook National University, Daegu, Republic of Korea.
authors.forename: Myung-Sook
authors.initials: MS
authors.lastname: Choi
authors.forename: Won-Ha
authors.initials: WH
authors.lastname: Lee
authors.forename: Eun-Young
authors.initials: EY
authors.lastname: Kwon
authors.forename: Mi Ae
authors.initials: MA
authors.lastname: Kang
authors.forename: Mi-Kyung
authors.initials: MK
authors.lastname: Lee
authors.forename: Yong Bok
authors.initials: YB
authors.lastname: Park
authors.forename: Seon-Min
authors.initials: SM
authors.lastname: Jeon
mesh_terms: D002460:Cell Line; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D016207:Cytokines / Q000032:analysis*; D004305:Dose-Response Relationship, Drug; D006801:Humans; D007294:Inositol / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism; D008055:Lipids / Q000032:analysis; D008077:Lipoproteins, LDL / Q000494:pharmacology*; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D051116:Receptors, Scavenger / Q000032:analysis*; D013025:Glycine max / Q000737:chemistry*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D016207:Cytokines; D053583:Interleukin-1beta; D016209:Interleukin-8; D008055:Lipids; D008077:Lipoproteins, LDL; D012333:RNA, Messenger; D051116:Receptors, Scavenger; D014409:Tumor Necrosis Factor-alpha; C099252:oxidized low density lipoprotein; C021730:pinitol; D007294:Inositol; D020780:Matrix Metalloproteinase 9